Review

bmp10 (R&D Systems)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems bmp10

EC-specific overactivation of mTORC1 reduces incidence and thickness of AVMs induced by blocking antibodies. A . Time scheme for administration of tamoxifen, BMP9/10 blocking antibodies (bAbs)/Isotype <t>IgG,</t> and sample collection. B . Representative pictures showing retinal vasculatures of control (Cre-) and Tsc1 iECKO mice treated with IgGs or anti-BMP9/10 antibodies (Abs). Arrows indicate AVMs. C . Quantification of number of AVMs per retina of Control ( n = 5 mice) and Tsc1 iECKO ( n = 5 mice) mice treated with anti-BMP9/10 Abs. D . Quantification of AVM thickness in Control ( n = 5 mice) and Tsc1 iECKO mice ( n = 3) treated with IgGs or anti-BMP9/10 Abs. E . Central retinal vasculatures of control (Cre-) and Tsc1 iECKO mice, treated with anti-BMP9/10 Abs, immunolabelled for CD31, p-RPS6, and YFP (indicative of recombination). F . Quantification of the ratio of the p-RPS6 + area within the CD31 + area to the complete CD31 + area ( F ), as well as the p-RPS6 + area outside the CD31 + area to the complete non-vascular area ( G ) of central retinas of Control ( n = 3 mice) and Tsc1 iECKO ( n = 3 mice) mice treated with anti-BMP9/10 Abs. Note the vascular specific increase of p-RPS6, indicative of EC-specific mTORC1 overactivation. All data was analysed by two-tailed unpaired t-test with Welch’s correction. Bars indicate mean ± s.d. * p < 0.05

Bmp10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bmp10/product/R&D Systems
Average 93 stars, based on 62 article reviews

bmp10 - by Bioz Stars, 2026-03

93/100 stars

Images

1) Product Images from "Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT"

Article Title: Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT

Journal: Angiogenesis

doi: 10.1007/s10456-024-09961-5

Figure Legend Snippet: EC-specific overactivation of mTORC1 reduces incidence and thickness of AVMs induced by blocking antibodies. A . Time scheme for administration of tamoxifen, BMP9/10 blocking antibodies (bAbs)/Isotype IgG, and sample collection. B . Representative pictures showing retinal vasculatures of control (Cre-) and Tsc1 iECKO mice treated with IgGs or anti-BMP9/10 antibodies (Abs). Arrows indicate AVMs. C . Quantification of number of AVMs per retina of Control ( n = 5 mice) and Tsc1 iECKO ( n = 5 mice) mice treated with anti-BMP9/10 Abs. D . Quantification of AVM thickness in Control ( n = 5 mice) and Tsc1 iECKO mice ( n = 3) treated with IgGs or anti-BMP9/10 Abs. E . Central retinal vasculatures of control (Cre-) and Tsc1 iECKO mice, treated with anti-BMP9/10 Abs, immunolabelled for CD31, p-RPS6, and YFP (indicative of recombination). F . Quantification of the ratio of the p-RPS6 + area within the CD31 + area to the complete CD31 + area ( F ), as well as the p-RPS6 + area outside the CD31 + area to the complete non-vascular area ( G ) of central retinas of Control ( n = 3 mice) and Tsc1 iECKO ( n = 3 mice) mice treated with anti-BMP9/10 Abs. Note the vascular specific increase of p-RPS6, indicative of EC-specific mTORC1 overactivation. All data was analysed by two-tailed unpaired t-test with Welch’s correction. Bars indicate mean ± s.d. * p < 0.05

Techniques Used: Blocking Assay, Control, Two Tailed Test

Image Search Results

Journal: Angiogenesis

Article Title: Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT

doi: 10.1007/s10456-024-09961-5

Figure Lengend Snippet: EC-specific overactivation of mTORC1 reduces incidence and thickness of AVMs induced by blocking antibodies. A . Time scheme for administration of tamoxifen, BMP9/10 blocking antibodies (bAbs)/Isotype IgG, and sample collection. B . Representative pictures showing retinal vasculatures of control (Cre-) and Tsc1 iECKO mice treated with IgGs or anti-BMP9/10 antibodies (Abs). Arrows indicate AVMs. C . Quantification of number of AVMs per retina of Control ( n = 5 mice) and Tsc1 iECKO ( n = 5 mice) mice treated with anti-BMP9/10 Abs. D . Quantification of AVM thickness in Control ( n = 5 mice) and Tsc1 iECKO mice ( n = 3) treated with IgGs or anti-BMP9/10 Abs. E . Central retinal vasculatures of control (Cre-) and Tsc1 iECKO mice, treated with anti-BMP9/10 Abs, immunolabelled for CD31, p-RPS6, and YFP (indicative of recombination). F . Quantification of the ratio of the p-RPS6 + area within the CD31 + area to the complete CD31 + area ( F ), as well as the p-RPS6 + area outside the CD31 + area to the complete non-vascular area ( G ) of central retinas of Control ( n = 3 mice) and Tsc1 iECKO ( n = 3 mice) mice treated with anti-BMP9/10 Abs. Note the vascular specific increase of p-RPS6, indicative of EC-specific mTORC1 overactivation. All data was analysed by two-tailed unpaired t-test with Welch’s correction. Bars indicate mean ± s.d. * p < 0.05

Article Snippet: Pups were treated with mouse monoclonal antibodies against BMP9 and BMP10 (15 mg/kg, IgG2b, MAB3209; 15 mg/kg, IgG2a, MAB2926; R&D Systems, respectively) or isotype control antibodies (15 mg/kg, IgG2b, MAB004; 15 mg/kg, IgG2a, MAB003; R&D Systems, respectively) at P3, P4 and P5 and tissues were harvested at P6.

Techniques: Blocking Assay, Control, Two Tailed Test

Up-regulated local BMP10 expression in the right atrium of precPH patients. ( A ) Quantification of the relative BMP10 mRNA expression in control ( n = 9) and precPH ( n = 5 CTEPH) RA tissues. ( B and C ) Quantification of total RA BMP10 fluorescent area and RA cardiomyocytes BMP10 intensity levels in control ( n = 6) and precPH ( n = 4 PAH) paraffin-embedded RA tissue sections stained against BMP10, respectively. Representative immunofluorescent stainings of BMP10, Ulex-rhodamine (Ulex, endothelium), and cardiac TroponinT (cTnT, myocardium) in the negative control sample for anti-rabbit Alexa488 and anti-mouse Alexa647 ( D ), in the control ( E ), and in the precPH ( F ) RA tissues at 60×-oil magnification. ( D’–F’ ) Alexa488 single-channel images from the stainings in ( D–F ). ( E ′′ and F′′ ) Zoom-in images from ( E′ and F′ ) to appreciate the sarcomeric pattern of the BMP10 staining in the cardiomyocytes and the homogeneous staining in the vessels. Scale bars = 50 μm. Brightness and contrast for the Alexa488 channel have not been modified. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using an independent sample t -test.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Up-regulated local BMP10 expression in the right atrium of precPH patients. ( A ) Quantification of the relative BMP10 mRNA expression in control ( n = 9) and precPH ( n = 5 CTEPH) RA tissues. ( B and C ) Quantification of total RA BMP10 fluorescent area and RA cardiomyocytes BMP10 intensity levels in control ( n = 6) and precPH ( n = 4 PAH) paraffin-embedded RA tissue sections stained against BMP10, respectively. Representative immunofluorescent stainings of BMP10, Ulex-rhodamine (Ulex, endothelium), and cardiac TroponinT (cTnT, myocardium) in the negative control sample for anti-rabbit Alexa488 and anti-mouse Alexa647 ( D ), in the control ( E ), and in the precPH ( F ) RA tissues at 60×-oil magnification. ( D’–F’ ) Alexa488 single-channel images from the stainings in ( D–F ). ( E ′′ and F′′ ) Zoom-in images from ( E′ and F′ ) to appreciate the sarcomeric pattern of the BMP10 staining in the cardiomyocytes and the homogeneous staining in the vessels. Scale bars = 50 μm. Brightness and contrast for the Alexa488 channel have not been modified. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using an independent sample t -test.

Article Snippet: RA paraffin-embedded tissue from controls ( n = 6) and precPH patients ( n = 4 PAH) was stained using an antibody against BMP10 (diluted 1:200; Biorbyt, United Kingdom), cardiac Troponin T (cTnT, diluted 1:500; Abcam, United Kingdom), phosphorylated receptor-regulated Smad1, Smad5, and Smad8 (pSMAD1/5/8, diluted 1:200; Cell Signaling, United States of America), and inhibitor of differentiation 3 (ID3, diluted 1:50; Santa Cruz Biotechnologies, United States of America).

Techniques: Expressing, Control, Staining, Negative Control, Modification, Transformation Assay

Up-regulated local BMP10 activity in the right atrium of precPH patients. ( A ) Quantification of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( B and C ) Representative immunofluorescent staining of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. ( D ) Quantification of positive ID3 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( E and F ) Representative immunofluorescent staining of positive ID3 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. Arrowheads indicate positive pSMAD1/5/8 and ID3 nuclei. Zoom-in images are included within ( B , C , E , and F ). Nuclei were counterstained with Hoechst 33342 and vessels with Ulex-rhodamine ( B , C , E , and F ). Negative control images are shown in , . Scale bars = 50 μm. Vascular and non-vascular measurements are plotted with their own Y -axis on the left or right side, respectively. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using a Wilcoxon rank-sum test (in A and D ).

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Up-regulated local BMP10 activity in the right atrium of precPH patients. ( A ) Quantification of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( B and C ) Representative immunofluorescent staining of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. ( D ) Quantification of positive ID3 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( E and F ) Representative immunofluorescent staining of positive ID3 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. Arrowheads indicate positive pSMAD1/5/8 and ID3 nuclei. Zoom-in images are included within ( B , C , E , and F ). Nuclei were counterstained with Hoechst 33342 and vessels with Ulex-rhodamine ( B , C , E , and F ). Negative control images are shown in , . Scale bars = 50 μm. Vascular and non-vascular measurements are plotted with their own Y -axis on the left or right side, respectively. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using a Wilcoxon rank-sum test (in A and D ).

Techniques: Activity Assay, Staining, Control, Negative Control, Transformation Assay

Higher BMP10 plasma levels in precPH patients compared with controls. ( A and B ) BMP10 protein circulating plasma levels in precPH patients ( n = 48) and subgroups ( n = 48: 22 iPAH, 14 hPAH, and 12 CTEPH), respectively, vs. controls ( n = 16). ( C and D ) BMP9 protein circulating plasma levels in precPH patients ( n = 45) and subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). ( E and F ) Correlation between BMP10 and BMP9 plasma levels in precPH patients ( n = 45) or subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). Logarithmic Y -axis is used in graphs ( A – D ). Data in ( A and B ) are y + 1 for logarithmic scale transformation. Normality of data was checked and transformed if needed. Statistical differences between precPH patients or precPH subgroups and controls were tested with an independent sample t -test or a one-way ANOVA, respectively. Associations were tested with univariate linear regression analysis.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Higher BMP10 plasma levels in precPH patients compared with controls. ( A and B ) BMP10 protein circulating plasma levels in precPH patients ( n = 48) and subgroups ( n = 48: 22 iPAH, 14 hPAH, and 12 CTEPH), respectively, vs. controls ( n = 16). ( C and D ) BMP9 protein circulating plasma levels in precPH patients ( n = 45) and subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). ( E and F ) Correlation between BMP10 and BMP9 plasma levels in precPH patients ( n = 45) or subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). Logarithmic Y -axis is used in graphs ( A – D ). Data in ( A and B ) are y + 1 for logarithmic scale transformation. Normality of data was checked and transformed if needed. Statistical differences between precPH patients or precPH subgroups and controls were tested with an independent sample t -test or a one-way ANOVA, respectively. Associations were tested with univariate linear regression analysis.

Techniques: Clinical Proteomics, Transformation Assay

BMP10 transcriptional activity in precPH patients and controls. ( A ) Schematic explanation of the BRE-LUC reporter assay to determine BMP transcriptional activity in venous serum. Specific trap antibodies targeting BMP9 or BMP9 and BMP10 are used to assess BMP10 activity. Created with BioRender.com. B ) Relative BMP transcriptional activity as a luciferase read-out from the HMEC-BRE-LUC, endothelial cells expressing a BMP-specific luciferase reporter, in control ( n = 15) and precPH subgroups ( n = 21 iPAH, n = 13 hPAH, and n = 11 CTEPH) after incubation with phosphate-buffered saline (PBS) (baseline), anti-BMP9, or ALK1-Fc (inhibition of BMP9 and BMP10). ( C ) BMP10 activity in controls and precPH subgroups has been calculated from the subtraction of anti-BMP9 and ALK1-Fc to total BMP activity. Normality of data was checked and transformed if needed. Statistical differences between precPH patients and controls, and between baseline conditions and trap antibodies, were tested with an independent sample t -test or a one-way ANOVA, after which pairwise t -testing with Bonferroni correction was applied, respectively.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: BMP10 transcriptional activity in precPH patients and controls. ( A ) Schematic explanation of the BRE-LUC reporter assay to determine BMP transcriptional activity in venous serum. Specific trap antibodies targeting BMP9 or BMP9 and BMP10 are used to assess BMP10 activity. Created with BioRender.com. B ) Relative BMP transcriptional activity as a luciferase read-out from the HMEC-BRE-LUC, endothelial cells expressing a BMP-specific luciferase reporter, in control ( n = 15) and precPH subgroups ( n = 21 iPAH, n = 13 hPAH, and n = 11 CTEPH) after incubation with phosphate-buffered saline (PBS) (baseline), anti-BMP9, or ALK1-Fc (inhibition of BMP9 and BMP10). ( C ) BMP10 activity in controls and precPH subgroups has been calculated from the subtraction of anti-BMP9 and ALK1-Fc to total BMP activity. Normality of data was checked and transformed if needed. Statistical differences between precPH patients and controls, and between baseline conditions and trap antibodies, were tested with an independent sample t -test or a one-way ANOVA, after which pairwise t -testing with Bonferroni correction was applied, respectively.

Techniques: Activity Assay, Reporter Assay, Luciferase, Expressing, Control, Incubation, Saline, Inhibition, Transformation Assay

$Patients with more right atrial dilatation, reduced RV ejection fraction, and higher NT-proBNP have higher levels of circulation BMP10 activity. ( A and B ) BMP10 transcriptional activity in precPH patients with RA or RV dilation, respectively. ( C–E ) BMP10 transcriptional activity in precPH patients with high RAP, reduced RVEF, or high NT-proBNP, respectively. PrecPH patients were stratified according to RA volume (>79 mL/mm 2 for male patients or >69 mL/mm 2 for female patients), RV end-diastolic volume index (≥109 mL/mm 2 for males, and ≥97 mL/mm 2 for females), RAP (>14 mmHg), RVEF (<35%), and NT-proBNP levels (>1100 ng/L). Normality of data was checked and transformed if needed. Statistical differences between both groups were tested with an independent samples t -test.$

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Patients with more right atrial dilatation, reduced RV ejection fraction, and higher NT-proBNP have higher levels of circulation BMP10 activity. ( A and B ) BMP10 transcriptional activity in precPH patients with RA or RV dilation, respectively. ( C–E ) BMP10 transcriptional activity in precPH patients with high RAP, reduced RVEF, or high NT-proBNP, respectively. PrecPH patients were stratified according to RA volume (>79 mL/mm 2 for male patients or >69 mL/mm 2 for female patients), RV end-diastolic volume index (≥109 mL/mm 2 for males, and ≥97 mL/mm 2 for females), RAP (>14 mmHg), RVEF (<35%), and NT-proBNP levels (>1100 ng/L). Normality of data was checked and transformed if needed. Statistical differences between both groups were tested with an independent samples t -test.

Techniques: Activity Assay, Transformation Assay

Effect of pressure unloading on BMP10 activity in precPH patients. ( A ) Serum relative BMP activity at baseline and post-PEA in CTEPH patients. Incubation with anti-BMP9 only blocked BMP9 activity, while ALK1-Fc blocked both BMP9 and BMP10 activities. ( B ) Calculated BMP10 transcriptional activity at baseline and post-PEA ( n = 13), respectively. BMP10 transcriptional activity is calculated by subtracting BMP activity values after incubation with the trap antibodies. Normality of data was checked and transformed if needed. Statistical differences between baseline conditions and trap antibodies, and between baseline and post-PEA, were tested with an independent sample t -test.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Effect of pressure unloading on BMP10 activity in precPH patients. ( A ) Serum relative BMP activity at baseline and post-PEA in CTEPH patients. Incubation with anti-BMP9 only blocked BMP9 activity, while ALK1-Fc blocked both BMP9 and BMP10 activities. ( B ) Calculated BMP10 transcriptional activity at baseline and post-PEA ( n = 13), respectively. BMP10 transcriptional activity is calculated by subtracting BMP activity values after incubation with the trap antibodies. Normality of data was checked and transformed if needed. Statistical differences between baseline conditions and trap antibodies, and between baseline and post-PEA, were tested with an independent sample t -test.

Techniques: Activity Assay, Incubation, Transformation Assay

(A) BMP10 mRNA abundance from spontaneously beating vEHT, spontaneously beating aEHT, and aEHT paced at 3 Hz for 7 days (+, blue, filled bars; RT-qPCR, n=3-4/1). (B) BMP10 in media from aEHT as in (A), collected after 48 h of aEHT culture (day 5-7, ELISA, n=4-6/1). One-way ANOVA followed by Tukey’s multiple comparisons test, p adj reported for all comparisons.

Journal: medRxiv

Article Title: High rate triggers increased atrial release of BMP10, a biomarker for atrial fibrillation and stroke, which affects ventricular cardiomyocytes

doi: 10.1101/2025.02.24.25322820

Figure Lengend Snippet: (A) BMP10 mRNA abundance from spontaneously beating vEHT, spontaneously beating aEHT, and aEHT paced at 3 Hz for 7 days (+, blue, filled bars; RT-qPCR, n=3-4/1). (B) BMP10 in media from aEHT as in (A), collected after 48 h of aEHT culture (day 5-7, ELISA, n=4-6/1). One-way ANOVA followed by Tukey’s multiple comparisons test, p adj reported for all comparisons.

Article Snippet: BMP10 in culture media was quantified by ELISA according to manufacturer’s instructions (EK18108, Human BMP-10 ELISA kit PicoKine, Boster, Pleasanton, USA).

Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

(A) AEHTs were paced at 5 Hz for 24 h or left unpaced (B-C, n=5/1). First medium sample taken directly after pacing, second sample 24 h after the end of pacing (post-pacing) or 24 h after unpaced control culture. Quantification of (B) BMP10 and (C) high-sensitivity troponin I (hsTnI) as a marker for cell damage, N-terminal pro-brain natriuretic peptide (NT-proBNP) as a marker for cardiomyocyte stress and glucose for verification of fast pacing by higher glucose consumption in fast-beating EHTs. Data show glucose concentrations remaining after 24 h of culture. One-way ANOVA followed by Šidák’s multiple comparisons test. Adjusted p-values are reported. (D) AEHTs were continuously optically paced for 5, 10 and 15 days at 4.5 Hz (E-F). (E) BMP10 concentration in aEHT medium (accumulated during 48 h) throughout the protocol. Paired T-test, fast-paced vs controls. (F) Relative BMP10 and BNP protein abundance in aEHTs after culture, analyzed by mass spectrometry-based proteomics after 15 days of continuous fast pacing. Student’s T-test, n=3 per group. Contractility data for quality control can be found in the supplement (Supplementary Fig. S2). BNP: Brain natriuretic peptide; Ctrl: Control; NT: Non-transduced; t0: time point 0 at start of protocol. 24 h: 24 h after pacing initiation, 48 h: 48 h after pacing initiation and 24 h after switching back to intrinsic rate.

Journal: medRxiv

Article Title: High rate triggers increased atrial release of BMP10, a biomarker for atrial fibrillation and stroke, which affects ventricular cardiomyocytes

doi: 10.1101/2025.02.24.25322820

Figure Lengend Snippet: (A) AEHTs were paced at 5 Hz for 24 h or left unpaced (B-C, n=5/1). First medium sample taken directly after pacing, second sample 24 h after the end of pacing (post-pacing) or 24 h after unpaced control culture. Quantification of (B) BMP10 and (C) high-sensitivity troponin I (hsTnI) as a marker for cell damage, N-terminal pro-brain natriuretic peptide (NT-proBNP) as a marker for cardiomyocyte stress and glucose for verification of fast pacing by higher glucose consumption in fast-beating EHTs. Data show glucose concentrations remaining after 24 h of culture. One-way ANOVA followed by Šidák’s multiple comparisons test. Adjusted p-values are reported. (D) AEHTs were continuously optically paced for 5, 10 and 15 days at 4.5 Hz (E-F). (E) BMP10 concentration in aEHT medium (accumulated during 48 h) throughout the protocol. Paired T-test, fast-paced vs controls. (F) Relative BMP10 and BNP protein abundance in aEHTs after culture, analyzed by mass spectrometry-based proteomics after 15 days of continuous fast pacing. Student’s T-test, n=3 per group. Contractility data for quality control can be found in the supplement (Supplementary Fig. S2). BNP: Brain natriuretic peptide; Ctrl: Control; NT: Non-transduced; t0: time point 0 at start of protocol. 24 h: 24 h after pacing initiation, 48 h: 48 h after pacing initiation and 24 h after switching back to intrinsic rate.

Article Snippet: BMP10 in culture media was quantified by ELISA according to manufacturer’s instructions (EK18108, Human BMP-10 ELISA kit PicoKine, Boster, Pleasanton, USA).

Techniques: Control, Marker, Concentration Assay, Mass Spectrometry

Log10-transformed (A) BMP10 and (B) NT-proBNP plasma concentrations by rhythm at blood draw. Protein concentrations were quantified in plasma of patients without AF (True SR; sinus rhythm), with diagnosed atrial AF but in SR at the day of blood draw (AF in SR) and patients with AF in AF at the day of blood draw. n=True SR: 814, AF in SR: 254, AF in AF: 302. Median and quartiles are depicted. One-way ANOVA followed by Tukey’s multiple comparisons test, p adj reported for all comparisons.

Journal: medRxiv

Article Title: High rate triggers increased atrial release of BMP10, a biomarker for atrial fibrillation and stroke, which affects ventricular cardiomyocytes

doi: 10.1101/2025.02.24.25322820

Figure Lengend Snippet: Log10-transformed (A) BMP10 and (B) NT-proBNP plasma concentrations by rhythm at blood draw. Protein concentrations were quantified in plasma of patients without AF (True SR; sinus rhythm), with diagnosed atrial AF but in SR at the day of blood draw (AF in SR) and patients with AF in AF at the day of blood draw. n=True SR: 814, AF in SR: 254, AF in AF: 302. Median and quartiles are depicted. One-way ANOVA followed by Tukey’s multiple comparisons test, p adj reported for all comparisons.

Article Snippet: BMP10 in culture media was quantified by ELISA according to manufacturer’s instructions (EK18108, Human BMP-10 ELISA kit PicoKine, Boster, Pleasanton, USA).

Techniques: Transformation Assay

(A) Expression of BMP10 and its known receptors in different cell populations of the adult human heart derived from snRNAseq analyses , via https://singlecell.broadinstitute.org/single_cell . (B) BMP10 receptor expression in vEHT (RNA sequencing, n=5/1). (C) Relative mRNA abundance of ALK3 and BMPR2 in vEHT and aEHT, RT-qPCR, n=3-4/1. Unpaired T-test, ***p<0.001.

Journal: medRxiv

Article Title: High rate triggers increased atrial release of BMP10, a biomarker for atrial fibrillation and stroke, which affects ventricular cardiomyocytes

doi: 10.1101/2025.02.24.25322820

Figure Lengend Snippet: (A) Expression of BMP10 and its known receptors in different cell populations of the adult human heart derived from snRNAseq analyses , via https://singlecell.broadinstitute.org/single_cell . (B) BMP10 receptor expression in vEHT (RNA sequencing, n=5/1). (C) Relative mRNA abundance of ALK3 and BMPR2 in vEHT and aEHT, RT-qPCR, n=3-4/1. Unpaired T-test, ***p<0.001.

Article Snippet: BMP10 in culture media was quantified by ELISA according to manufacturer’s instructions (EK18108, Human BMP-10 ELISA kit PicoKine, Boster, Pleasanton, USA).

Techniques: Expressing, Derivative Assay, RNA Sequencing, Quantitative RT-PCR

RT‐qPCR was used to detect the expression levels of key genes, including BMP10, HAMP, TRIM5, MLANA, PTPRN2 and AVP. *** p < 0.001 versus Control group. RT‐qPCR, reverse transcription quantitative PCR.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: RT‐qPCR was used to detect the expression levels of key genes, including BMP10, HAMP, TRIM5, MLANA, PTPRN2 and AVP. *** p < 0.001 versus Control group. RT‐qPCR, reverse transcription quantitative PCR.

Article Snippet: Three types of small interfering RNA (siRNA) targeting BMP10 (si‐BMP10‐1, si‐BMP10‐2 and si‐BMP10‐3) and a negative control (si‐NC) were synthesised by RiboBio (Guangzhou, China).

Techniques: Quantitative RT-PCR, Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction

BMP10 knockdown inhibited apoptosis, inflammation and cell adhesion in CMECs. (A) After the CMECs were transfected with si‐BMP10‐1, si‐BMP10‐2 and si‐BMP10‐3, RT‐qPCR was used to assess the knockdown efficiency of BMP10. ΔΔΔ p < 0.001 versus si‐NC group. (B) Cell viability in the control, LPS, LPS + si‐NC and LPS + si‐ BMP10 groups was assessed by CCK‐8 assay. (C) Apoptosis was measured using flow cytometry in the four groups. (D) Levels of inflammatory factors, including IL‐6, MCP‐1, IFN‐β and CCL11 were detected by ELISA assay. (E) Protein levels of cell adhesion molecules, including VCAM‐1 and ICAM‐1were evaluated by western blot analysis. *** p < 0.001 versus control group; ## p < 0.01 hematoxylin and eosin, ### p < 0.001 versus LPS + si‐NC group. CMECs, cardiac microvascular endothelial cells; CCK‐8, cell counting kit‐8; ELISA assay, enzyme‐linked immunosorbent assay; RT‐qPCR, reverse transcription quantitative PCR.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: BMP10 knockdown inhibited apoptosis, inflammation and cell adhesion in CMECs. (A) After the CMECs were transfected with si‐BMP10‐1, si‐BMP10‐2 and si‐BMP10‐3, RT‐qPCR was used to assess the knockdown efficiency of BMP10. ΔΔΔ p < 0.001 versus si‐NC group. (B) Cell viability in the control, LPS, LPS + si‐NC and LPS + si‐ BMP10 groups was assessed by CCK‐8 assay. (C) Apoptosis was measured using flow cytometry in the four groups. (D) Levels of inflammatory factors, including IL‐6, MCP‐1, IFN‐β and CCL11 were detected by ELISA assay. (E) Protein levels of cell adhesion molecules, including VCAM‐1 and ICAM‐1were evaluated by western blot analysis. *** p < 0.001 versus control group; ## p < 0.01 hematoxylin and eosin, ### p < 0.001 versus LPS + si‐NC group. CMECs, cardiac microvascular endothelial cells; CCK‐8, cell counting kit‐8; ELISA assay, enzyme‐linked immunosorbent assay; RT‐qPCR, reverse transcription quantitative PCR.

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Control, CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Western Blot, Cell Counting, Reverse Transcription, Real-time Polymerase Chain Reaction

Knockdown of BMP10 ameliorated pathological changes and inhibited apoptosis and inflammatory responses in SIMI mice model ( n = 6 mice per group). (A) Histopathological changes in the cardiac tissues of mice were examined using HE staining in the control, LPS, LPS + AAV‐NC and LPS + AAV‐BMP10 groups. Magnification: 400×, Scale: 100 μm. (B) Fluorescent TUNEL labelling (red) and DAPI nuclear staining (blue) were employed to respectively detect apoptotic cells and visualise cell nuclei. (C) The ELISA assay was employed to measure the levels of inflammatory factors (IL‐6, MCP‐1, IFN‐β and CCL11) in the SIMI mice model. *** p < 0.001 versus control group: ### p < 0.001 versus LPS + AAV‐NC group. ELISA, enzyme‐linked immunosorbent assay; HE staining, hematoxylin and eosin staining; SIMI, sepsis‐induced myocardial injury; TUNEL, terminal deoxynucleotidyl‐transferase‐mediated dUTP nick end labelling.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: Knockdown of BMP10 ameliorated pathological changes and inhibited apoptosis and inflammatory responses in SIMI mice model ( n = 6 mice per group). (A) Histopathological changes in the cardiac tissues of mice were examined using HE staining in the control, LPS, LPS + AAV‐NC and LPS + AAV‐BMP10 groups. Magnification: 400×, Scale: 100 μm. (B) Fluorescent TUNEL labelling (red) and DAPI nuclear staining (blue) were employed to respectively detect apoptotic cells and visualise cell nuclei. (C) The ELISA assay was employed to measure the levels of inflammatory factors (IL‐6, MCP‐1, IFN‐β and CCL11) in the SIMI mice model. *** p < 0.001 versus control group: ### p < 0.001 versus LPS + AAV‐NC group. ELISA, enzyme‐linked immunosorbent assay; HE staining, hematoxylin and eosin staining; SIMI, sepsis‐induced myocardial injury; TUNEL, terminal deoxynucleotidyl‐transferase‐mediated dUTP nick end labelling.

Techniques: Knockdown, Staining, Control, TUNEL Assay, Enzyme-linked Immunosorbent Assay

Knockdown of BMP10 inhibited cell adhesion and immune cell infiltration in SIMI mice model. (A) Western blot was used to examine the expression levels of cell adhesion molecules VCAM‐1 and ICAM‐1. (B) IHC staining analysis of peripheral immune cell infiltration in mouse heart. Magnification: 400×, Scale bar: 20 μm. Red arrows indicate macrophages. (C) ELISA assay was performed to quantify the expression levels of myocardial injury markers (CK‐MB, LDH and cTnT) in the mouse heart. *** p < 0.001 versus control group; ## p < 0.01, ### p < 0.001 versus LPS + AAV‐NC group. ELISA, enzyme‐linked immunosorbent assay; IHC staining, immunohistochemical staining; SIMI, sepsis‐induced myocardial injury.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: Knockdown of BMP10 inhibited cell adhesion and immune cell infiltration in SIMI mice model. (A) Western blot was used to examine the expression levels of cell adhesion molecules VCAM‐1 and ICAM‐1. (B) IHC staining analysis of peripheral immune cell infiltration in mouse heart. Magnification: 400×, Scale bar: 20 μm. Red arrows indicate macrophages. (C) ELISA assay was performed to quantify the expression levels of myocardial injury markers (CK‐MB, LDH and cTnT) in the mouse heart. *** p < 0.001 versus control group; ## p < 0.01, ### p < 0.001 versus LPS + AAV‐NC group. ELISA, enzyme‐linked immunosorbent assay; IHC staining, immunohistochemical staining; SIMI, sepsis‐induced myocardial injury.

Techniques: Knockdown, Western Blot, Expressing, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Control, Immunohistochemical staining, Staining

KEGG functional enrichment analysis for BMP10‐related immune infiltration DEGs in SIMI. (A) Histogram of KEGG functional enrichment analysis. (B) Bubble plot of KEGG functional enrichment analysis. KEGG, Kyoto Encyclopedia of Genes and Genomes; SIMI, sepsis‐induced myocardial injury.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: KEGG functional enrichment analysis for BMP10‐related immune infiltration DEGs in SIMI. (A) Histogram of KEGG functional enrichment analysis. (B) Bubble plot of KEGG functional enrichment analysis. KEGG, Kyoto Encyclopedia of Genes and Genomes; SIMI, sepsis‐induced myocardial injury.

Techniques: Functional Assay

Knockdown of BMP10 suppressed SIMI development by suppressing the HIF‐1α pathway. (A) Cell viability in the control, LPS, LPS + si‐NC, LPS + si‐BMP10 and LPS + si‐BMP10 + Fenbendazole‐d3 groups was measured by CCK‐8 assay. (B) Flow cytometry was performed to assess apoptosis in five groups. (C) The levels of inflammatory factors (IL‐6, MCP‐1, IFN‐β and CCL11) were measured using the ELISA assay. (D) The expression levels of cell adhesion molecules VCAM‐1, ICAM‐1 and key proteins of the HIF‐1 pathway were assessed using western blot analysis. *** p < 0.001 versus control group; # p ＜0.05, ## p ＜0.01, ### p < 0.001 versus LPS + si‐NC group; & p < 0.05, && p < 0.01 and &&& p < 0.001 versus LPS + si‐BMP10 group. CCK‐8, cell counting kit‐8; ELISA, enzyme‐linked immunosorbent assay; SIMI, sepsis‐induced myocardial injury.

Journal: Journal of Cellular and Molecular Medicine

Article Title: BMP10 Knockdown Modulates Endothelial Cell Immunoreactivity by Inhibiting the HIF‐1α Pathway in the Sepsis‐Induced Myocardial Injury

doi: 10.1111/jcmm.70232

Figure Lengend Snippet: Knockdown of BMP10 suppressed SIMI development by suppressing the HIF‐1α pathway. (A) Cell viability in the control, LPS, LPS + si‐NC, LPS + si‐BMP10 and LPS + si‐BMP10 + Fenbendazole‐d3 groups was measured by CCK‐8 assay. (B) Flow cytometry was performed to assess apoptosis in five groups. (C) The levels of inflammatory factors (IL‐6, MCP‐1, IFN‐β and CCL11) were measured using the ELISA assay. (D) The expression levels of cell adhesion molecules VCAM‐1, ICAM‐1 and key proteins of the HIF‐1 pathway were assessed using western blot analysis. *** p < 0.001 versus control group; # p ＜0.05, ## p ＜0.01, ### p < 0.001 versus LPS + si‐NC group; & p < 0.05, && p < 0.01 and &&& p < 0.001 versus LPS + si‐BMP10 group. CCK‐8, cell counting kit‐8; ELISA, enzyme‐linked immunosorbent assay; SIMI, sepsis‐induced myocardial injury.

Techniques: Knockdown, Control, CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot, Cell Counting

Graphical representation of the experimental design. Experiment 1: Changes in pain sensitization and expressions of BMP10, ALK2, Smad1/5/8, phosphorylated Smad1/5/8, and GFAP after SNI in mice. Experiment 2: The effects of BMP10 siRNA on SNI-induced pain hypersensitivity and astrocytic activation. Experiment 3: The involvements of ALK2 in BMP10-induced pain hypersensitivity and astrocytic activation. Experiment 4: The effects of Smad1 siRNA on BMP10-induced pain hypersensitivity and astrocytic activation.

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Graphical representation of the experimental design. Experiment 1: Changes in pain sensitization and expressions of BMP10, ALK2, Smad1/5/8, phosphorylated Smad1/5/8, and GFAP after SNI in mice. Experiment 2: The effects of BMP10 siRNA on SNI-induced pain hypersensitivity and astrocytic activation. Experiment 3: The involvements of ALK2 in BMP10-induced pain hypersensitivity and astrocytic activation. Experiment 4: The effects of Smad1 siRNA on BMP10-induced pain hypersensitivity and astrocytic activation.

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Activation Assay

Intrathecal injection of BMP10 siRNA decreased the expression of BMP10 without conspicuous side effects. (A) qRT-PCR analysis showed the expression levels of BMP10 mRNA in the spinal cord of mice after intrathecal injection with the vehicle, NC siRNA, and BMP10 siRNA; (B, C) Western blot analysis showed the expression levels of BMP10 protein in the spinal cord of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA; (D, E) Paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL) of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA; (F) Representative movement traces in OFT tests of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA (G–I) Time in center zone, average speed, and total distance of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA. Data were presented as mean and SEM, BMP10 siRNA group versus Control group ** p < 0.01, *** p < 0.001; BMP10 siRNA group versus NC siRNA group ## p < 0.01, ### p < 0.001, n = 6.

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Intrathecal injection of BMP10 siRNA decreased the expression of BMP10 without conspicuous side effects. (A) qRT-PCR analysis showed the expression levels of BMP10 mRNA in the spinal cord of mice after intrathecal injection with the vehicle, NC siRNA, and BMP10 siRNA; (B, C) Western blot analysis showed the expression levels of BMP10 protein in the spinal cord of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA; (D, E) Paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL) of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA; (F) Representative movement traces in OFT tests of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA (G–I) Time in center zone, average speed, and total distance of mice after intrathecal injected with vehicle, NC siRNA, BMP10 siRNA. Data were presented as mean and SEM, BMP10 siRNA group versus Control group ** p < 0.01, *** p < 0.001; BMP10 siRNA group versus NC siRNA group ## p < 0.01, ### p < 0.001, n = 6.

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Injection, Expressing, Quantitative RT-PCR, Western Blot, Control

Intrathecal injection of BMP10 siRNA inhibited the SNI-induced pain hypersensitivity and astrocytic activation. (A, B) The time course of PWT and TWL in sham and SNI mice after intrathecal delivery of siRNAs; Data are presented as mean and SEM; SNI + NC siRNA group and SNI + BMP10 siRNA group versus Sham + NC siRNA *** p < 0.001; SNI + BMP10 siRNA versus SNI + NC siRNA group # p < 0.05 ## p < 0.01 (n = 12); (C, D) Western blot showed the expression levels of BMP10 and GFAP in the spinal cord of sham and SNI mice after intrathecal delivery of siRNAs on postoperative Day 14; (E, F) Immunofluorescence staining results showing the expression of GFAP in the spinal dorsal horn of sham and SNI mice after intrathecal delivery of siRNAs on postoperative Day 14 (scale bar = 100 μm/50 μm); Data are presented as mean and SEM; SNI + NC siRNA group and SNI + BMP10 siRNA group versus Sham + NC siRNA*** p < 0.001; SNI + BMP10 siRNA versus SNI + NC siRNA group # p < 0.05, ### p < 0.001 (n = 6).

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Intrathecal injection of BMP10 siRNA inhibited the SNI-induced pain hypersensitivity and astrocytic activation. (A, B) The time course of PWT and TWL in sham and SNI mice after intrathecal delivery of siRNAs; Data are presented as mean and SEM; SNI + NC siRNA group and SNI + BMP10 siRNA group versus Sham + NC siRNA *** p < 0.001; SNI + BMP10 siRNA versus SNI + NC siRNA group # p < 0.05 ## p < 0.01 (n = 12); (C, D) Western blot showed the expression levels of BMP10 and GFAP in the spinal cord of sham and SNI mice after intrathecal delivery of siRNAs on postoperative Day 14; (E, F) Immunofluorescence staining results showing the expression of GFAP in the spinal dorsal horn of sham and SNI mice after intrathecal delivery of siRNAs on postoperative Day 14 (scale bar = 100 μm/50 μm); Data are presented as mean and SEM; SNI + NC siRNA group and SNI + BMP10 siRNA group versus Sham + NC siRNA*** p < 0.001; SNI + BMP10 siRNA versus SNI + NC siRNA group # p < 0.05, ### p < 0.001 (n = 6).

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Injection, Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

Smad1 was pivotal in astrocytic activation in vitro . (A) qRT-PCR analysis showed the expression levels of Smad1 mRNA in cultured astrocytes transfected with siRNAs; (B) Western blot analysis showed the expression levels of Smad1 protein in cultured astrocytes transfected with siRNAs data are presented as mean and SEM, Smad1 siRNA group versus + Control group *** p < 0.001 (n = 6); (C) The purity of cultured astrocytes (scale bar = 200 μm); (D) The CCK assay showed the cell viability of cultured astrocytes; (E, F) Immunofluorescence staining results showed the expression of GFAP in cultured astrocytes transfected with siRNAs (scale bar = 50 μm); (G, H) Western blot showed the expressions of GFAP and p-Smad1/5/8 and in cultured cells; data are presented as mean and SEM, NC siRNA + Vehicle group versus NC siRNA + LPS group *** p < 0.001; NC siRNA + LPS group versus Smad1 siRNA + LPS group ### p < 0.001 (n = 6).

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Smad1 was pivotal in astrocytic activation in vitro . (A) qRT-PCR analysis showed the expression levels of Smad1 mRNA in cultured astrocytes transfected with siRNAs; (B) Western blot analysis showed the expression levels of Smad1 protein in cultured astrocytes transfected with siRNAs data are presented as mean and SEM, Smad1 siRNA group versus + Control group *** p < 0.001 (n = 6); (C) The purity of cultured astrocytes (scale bar = 200 μm); (D) The CCK assay showed the cell viability of cultured astrocytes; (E, F) Immunofluorescence staining results showed the expression of GFAP in cultured astrocytes transfected with siRNAs (scale bar = 50 μm); (G, H) Western blot showed the expressions of GFAP and p-Smad1/5/8 and in cultured cells; data are presented as mean and SEM, NC siRNA + Vehicle group versus NC siRNA + LPS group *** p < 0.001; NC siRNA + LPS group versus Smad1 siRNA + LPS group ### p < 0.001 (n = 6).

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Activation Assay, In Vitro, Quantitative RT-PCR, Expressing, Cell Culture, Transfection, Western Blot, Control, Immunofluorescence, Staining

Intrathecal injection of Smad1 siRNA knocked down the expression of Smad1 without obvious side effects. (A) qRT-PCR analysis showed the expression levels of Smad1 mRNA in the spinal cord of mice after intrathecal injection with vehicle, NC siRNA, Smad1 siRNA; (B, C) Western blot analysis showed the expression levels of Smad1 protein in the spinal cord of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA; (D, E) Paw withdrawal threshold (PWT) and Thermal withdrawal latency (TWL) of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA (F) Representative movement traces in OFT tests of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA (G–I) Time in center zone, average speed and total distance of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA. Data were presented as mean and SEM, Smad1 siRNA group versus Control group *** p < 0.001; Smad1 siRNA group versus NC siRNA group ### p < 0.001, n = 6.

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Intrathecal injection of Smad1 siRNA knocked down the expression of Smad1 without obvious side effects. (A) qRT-PCR analysis showed the expression levels of Smad1 mRNA in the spinal cord of mice after intrathecal injection with vehicle, NC siRNA, Smad1 siRNA; (B, C) Western blot analysis showed the expression levels of Smad1 protein in the spinal cord of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA; (D, E) Paw withdrawal threshold (PWT) and Thermal withdrawal latency (TWL) of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA (F) Representative movement traces in OFT tests of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA (G–I) Time in center zone, average speed and total distance of mice after intrathecal injected with vehicle, NC siRNA, Smad1 siRNA. Data were presented as mean and SEM, Smad1 siRNA group versus Control group *** p < 0.001; Smad1 siRNA group versus NC siRNA group ### p < 0.001, n = 6.

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Injection, Expressing, Quantitative RT-PCR, Western Blot, Control

Smad1 was involved in BMP10-induced pain hypersensitivity and astrocytic activation. (A, B) PWT and TWL of normal mice after intrathecal delivery of siRNA and BMP10 peptide; (C, D) Western blot showed the expressions of p-Smad1/5/8 and GFAP in the spinal cord of normal mice after intrathecal delivery of siRNA and BMP10 peptide; (E, F) immunofluorescence staining showed the expression of GFAP in the spinal dorsal horn of normal mice after the intrathecal delivery of siRNA and BMP10 peptide; (scale bar = 200 μm/50 μm); Data are presented as mean and SEM, NC siRNA + Vehicle group versus NC siRNA + BMP10 group *** p < 0.001; NC siRNA + BMP10 group versus Smad1 siRNA + BMP10 group # p < 0.05, ### p < 0.001 (n = 6).

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Smad1 was involved in BMP10-induced pain hypersensitivity and astrocytic activation. (A, B) PWT and TWL of normal mice after intrathecal delivery of siRNA and BMP10 peptide; (C, D) Western blot showed the expressions of p-Smad1/5/8 and GFAP in the spinal cord of normal mice after intrathecal delivery of siRNA and BMP10 peptide; (E, F) immunofluorescence staining showed the expression of GFAP in the spinal dorsal horn of normal mice after the intrathecal delivery of siRNA and BMP10 peptide; (scale bar = 200 μm/50 μm); Data are presented as mean and SEM, NC siRNA + Vehicle group versus NC siRNA + BMP10 group *** p < 0.001; NC siRNA + BMP10 group versus Smad1 siRNA + BMP10 group # p < 0.05, ### p < 0.001 (n = 6).

Article Snippet: For in vivo siRNA transfection, siRNA targeting BMP10, Smad1, and negative control (NC) siRNA were obtained from OBIO Technology (Shanghai, China).

Techniques: Activation Assay, Western Blot, Immunofluorescence, Staining, Expressing

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Article Snippet: Subsequently, the tissues were incubated with the primary antibodies for 12 h at 4°C as follows: mouse anti-GFAP antibody (1:200, ab279289, Abcam), mouse anti-CGRP antibody (1:500, ab81887, Abcam), mouse anti-c-fos antibody (1:1,000, ab208942, Abcam), mouse anti-Iba-1 antibody (1:200, ab283319, Abcam), rat anti-BMP10 antibody (1:200, 654319, Novus Biologicals, CO, United States) and rabbit anti-ALK2 antibody (1:100, PA5-114818, Thermo Fisher Scientific, MA, United States).

Techniques: Activation Assay

Expression levels of BMP10, GFAP in mouse ipsilateral spinal dorsal horn after SNI. (A, B) Western blot analysis showed the expression levels of BMP10 and GFAP in the ipsilateral (above) and contralateral (below) spinal dorsal horn of sham and SNI mice; (C, D) Immunofluorescence staining showed the expression of GFAP in the ipsilateral and contralateral spinal dorsal horn of sham and SNI mice (scale bar = 200 μm/50 μm); (E–G) Double immunofluorescence staining showed the coexpression of BMP10 (red) with GFAP (green) in the ipsilateral spinal dorsal horn of sham and SNI mice on postoperative Day 14 (scale bar = 200 μm/50 μm). Data are presented as mean and SEM; sham mice versus SNI mice on postoperative Days 7 and 14, *** p < 0.001 (n = 6).

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Expression levels of BMP10, GFAP in mouse ipsilateral spinal dorsal horn after SNI. (A, B) Western blot analysis showed the expression levels of BMP10 and GFAP in the ipsilateral (above) and contralateral (below) spinal dorsal horn of sham and SNI mice; (C, D) Immunofluorescence staining showed the expression of GFAP in the ipsilateral and contralateral spinal dorsal horn of sham and SNI mice (scale bar = 200 μm/50 μm); (E–G) Double immunofluorescence staining showed the coexpression of BMP10 (red) with GFAP (green) in the ipsilateral spinal dorsal horn of sham and SNI mice on postoperative Day 14 (scale bar = 200 μm/50 μm). Data are presented as mean and SEM; sham mice versus SNI mice on postoperative Days 7 and 14, *** p < 0.001 (n = 6).

Techniques: Expressing, Western Blot, Immunofluorescence, Staining, Double Immunofluorescence Staining

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Techniques: Injection, Expressing, Quantitative RT-PCR, Western Blot, Control

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Techniques: Injection, Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

Intrathecal injection of BMP peptide evoked pain hypersensitivity and astrocytic activation in normal mice (A, B) The time course of PWT and TWL in normal mice after intrathecal delivery of BMP10 peptide and vehicle; Data were presented as mean and SEM, 100 ng group and 1000 ng group versus Vehicle group * p < 0.05, ** p < 0.01, *** p < 0.001; n = 6; (C) Western blot showed the expression levels of GFAP in spinal cord of mice after intrathecal delivery of BMP10 peptide and vehicle; (D) Western blot showed the expression levels of BMP10 in spinal cord at different time points after intrathecal delivery of BMP10 peptide (100 ng); (E–H) Immunofluorescence staining results showing the expression of c-fos, CGRP, and Iba-1 in the spinal dorsal horn of mice after intrathecal delivery of BMP10 peptide and vehicle (scale bar = 200 μm/50 μm). Data were presented as mean and SEM, 100 ng group and 1,000 ng group versus Vehicle group ** p < 0.01, *** p < 0.001; n = 6.

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: Intrathecal injection of BMP peptide evoked pain hypersensitivity and astrocytic activation in normal mice (A, B) The time course of PWT and TWL in normal mice after intrathecal delivery of BMP10 peptide and vehicle; Data were presented as mean and SEM, 100 ng group and 1000 ng group versus Vehicle group * p < 0.05, ** p < 0.01, *** p < 0.001; n = 6; (C) Western blot showed the expression levels of GFAP in spinal cord of mice after intrathecal delivery of BMP10 peptide and vehicle; (D) Western blot showed the expression levels of BMP10 in spinal cord at different time points after intrathecal delivery of BMP10 peptide (100 ng); (E–H) Immunofluorescence staining results showing the expression of c-fos, CGRP, and Iba-1 in the spinal dorsal horn of mice after intrathecal delivery of BMP10 peptide and vehicle (scale bar = 200 μm/50 μm). Data were presented as mean and SEM, 100 ng group and 1,000 ng group versus Vehicle group ** p < 0.01, *** p < 0.001; n = 6.

Techniques: Injection, Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

ALK2 was involved in BMP10-induced pain hypersensitivity and astrocytic activation. (A, B) The time course of PWT and TWL in normal mice after intrathecal delivery of BMP10 peptide and reagents; Data are presented as mean and SEM, Vehicle group versus BMP10 group * p < 0.05, ** p < 0.01, *** p < 0.001; BMP10+ALK2-IN-2 group versus BMP group # p < 0.05, ## p < 0.01, ### p < 0.001 (n = 12); (C) Representative movement traces in OFT tests of mice after intrathecal delivery of BMP10 peptide and reagents; (D–F) Time in center zone, average speed and total distance of mice in open field after intrathecal delivery of BMP10 peptide and reagents; (G, H) immunofluorescence staining showed the expression of GFAP in the spinal dorsal horn after intrathecal delivery of BMP10 peptide and reagents (scale bar = 200/50 μm); (I) Western blot showed the expression of GFAP in the spinal cord after intrathecal delivery of BMP10 peptide and reagents; Data are presented as mean and SEM, Vehicle group versus BMP10 group * p < 0.05, ** p < 0.01, *** p < 0.001; BMP10+ ALK2-IN-2 group versus BMP group # p < 0.05, ## p < 0.01, ### p < 0.001 (n = 6).

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Figure Lengend Snippet: ALK2 was involved in BMP10-induced pain hypersensitivity and astrocytic activation. (A, B) The time course of PWT and TWL in normal mice after intrathecal delivery of BMP10 peptide and reagents; Data are presented as mean and SEM, Vehicle group versus BMP10 group * p < 0.05, ** p < 0.01, *** p < 0.001; BMP10+ALK2-IN-2 group versus BMP group # p < 0.05, ## p < 0.01, ### p < 0.001 (n = 12); (C) Representative movement traces in OFT tests of mice after intrathecal delivery of BMP10 peptide and reagents; (D–F) Time in center zone, average speed and total distance of mice in open field after intrathecal delivery of BMP10 peptide and reagents; (G, H) immunofluorescence staining showed the expression of GFAP in the spinal dorsal horn after intrathecal delivery of BMP10 peptide and reagents (scale bar = 200/50 μm); (I) Western blot showed the expression of GFAP in the spinal cord after intrathecal delivery of BMP10 peptide and reagents; Data are presented as mean and SEM, Vehicle group versus BMP10 group * p < 0.05, ** p < 0.01, *** p < 0.001; BMP10+ ALK2-IN-2 group versus BMP group # p < 0.05, ## p < 0.01, ### p < 0.001 (n = 6).

Techniques: Activation Assay, Immunofluorescence, Staining, Expressing, Western Blot

Journal: Frontiers in Pharmacology

Article Title: BMP10 accelerated spinal astrocytic activation in neuropathic pain via ALK2/smad1/5/8 signaling

doi: 10.3389/fphar.2024.1426121

Techniques: Activation Assay, Western Blot, Immunofluorescence, Staining, Expressing

Review

Structured Review

Images

1) Product Images from "Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT"

Similar Products

Image Search Results