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ang 1 7 (MedChemExpress)

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MedChemExpress ang 1 7
Ang 1 7, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ang+1+7/Talfirastide/10__1177_slash_14703203261440460-114-11-15
Average 95 stars, based on 26 article reviews

ang 1 7 - by Bioz Stars, 2026-10

95/100 stars

Images

Incubation:

Article Title: Angiotensin(1–7) activates MAS-1 and upregulates CFTR to promote insulin secretion in pancreatic β-cells: the association with type 2 diabetes
Article Snippet: .. To test the acute effect of Ang(1–7), cells were starved in fetal bovine serum (FBS)-free and glucose-free RPMI1640 medium for 2 h before treated with Ang(1–7) (0, 1 and 10 μM, Catalog# 51833-78-4, MedChemExpress, Monmouth Junction, NJ, USA) in Margo solution (NaCl 130 mM, KCl 5 mM, MgCl 2 1 mM, CaCl 2 2.5 mM, HEPES 20 mM and glucose 10 mM, with pH 7.4) for 15 min. For experiments related to the long-term effect of Ang(1–7), cells were treated with Ang(1–7) (0, 1 and 10 μM) with or without the MAS-1 inhibitor, A779 (10 μM), in growth medium for 24 h before the drugs were removed and cells were starved in FBS-free and glucose-free RPMI1640 medium for 2 h and subsequently incubated in the glucose-containing Margo solution with or without the CFTR inhibitor 172 (CFTRinh-172, 10 μM) for additional 15 min. .. The incubated Margo solution was then collected, removed cells by centrifugation and used in the insulin ELISA assay (Catalog# 10-1248-10, Mercodia) following the manufacturer’s instruction.

Article Title: Angiotensin(1–7) activates MAS-1 and upregulates CFTR to promote insulin secretion in pancreatic β-cells: the association with type 2 diabetes
Article Snippet: .. To test the acute effect of Ang(1–7), cells were starved in fetal bovine serum (FBS)free and glucose-free RPMI1640 medium for 2 h before treated with Ang(1–7) (0, 1 and 10 μM, Catalog# 51833- 78-4, MedChemExpress, Monmouth Junction, NJ, USA) in Margo solution (NaCl 130 mM, KCl 5 mM, MgCl2 1 mM, CaCl2 2.5 mM, HEPES 20 mM and glucose 10 mM, with pH 7.4) for 15 min. For experiments related to the longterm effect of Ang(1–7), cells were treated with Ang(1–7) (0, 1 and 10 μM) with or without the MAS-1 inhibitor, A779 (10 μM), in growth medium for 24 h before the drugs were removed and cells were starved in FBS-free and glucose-free RPMI1640 medium for 2 h and subsequently incubated in the glucose-containing Margo solution with or without the CFTR inhibitor 172 (CFTRinh-172, 10 μM) for additional 15 min. .. The incubated Margo solution was then collected, removed cells by centrifugation and used in the insulin ELISA assay (Catalog# 10-1248-10, Mercodia) following the manufacturer’s instruction.

Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor
Article Snippet: .. For pharmacological treatment, cells were first pretreated with 1 μM A‐779 (MCE, HY‐P0216, USA), 100 nM PD123319 (MCE, HY‐10259A, USA), or 100 nM Alamandine (MCE, HY‐P3108, USA) for 1 h, then incubated with 80 nM Ang‐(1–7) (MCE, HY‐12403, USA) for 2 h, and finally exposed to isoproterenol (ISO; Solarbio, II0200, China) at 10 μM for 24 h. ..

Concentration Assay:

Article Title: ACE2 Alleviates Endoplasmic Reticulum Stress and Protects against Pyroptosis by Regulating Ang1-7/Mas in Ventilator-Induced Lung Injury.
Article Snippet: .. Ang (1-7) (HY-12403, MedChemExpress, Monmouth Junction, NJ, USA) was added to the medium at a final concentration of 100 nmol/L for pretreatment over 12 h, with continuous intervention during CS. .. Tunicamycin (TM, HY-A0098, MedChemExpress, Monmouth Junction, NJ, USA) was added to the medium at a final concentration of 2 μg/mL to induce ERS.

Injection:

Article Title: ACE2 improves endothelial cell function and reduces acute lung injury by downregulating FAK expression.
Article Snippet: Endothelial cell (EC) barrier dysfunction and increased adhesion of immune inflammatory cells to ECs crucially contribute to acute lung injury (ALI).. Angiotensin-converting enzyme 2 (ACE2) is an essential regulator of the renin-angiotensin system (RAS) and exerts characteristic vasodilatory and anti-inflammatory effects.. SARS-COV2 infects the lungs by binding to ACE2, which can lead to dysregulation of ACE2 expression, further leading to ALI with predominantly vascular inflammation and eventually to more severe acute respiratory distress syndrome (ARDS).

Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor
Article Snippet: .. After 7 days' acclimatization, animals were randomized (blinded assessment) into five groups ( n = 6 per group) receiving daily Subcutaneous injection for 7 days [ , , ]:Ctrl: saline (Sanlian, Harbin, China); ISO: isoproterenol 5 mg/kg/day (Solarbio, II0200, Beijing, China; dissolved in DMSO); ISO + Ang‐(1–7): Ang‐(1–7) 576 μg/kg/day (MCE, HY‐12403, USA; in distilled water); ISO + Ang‐(1–7) + A‐779: A‐7791148 μg/kg/day (MCE, HY‐P0216, USA); ISO + Ang‐(1–7) + PD123319 : PD123319 5 mg/kg/day (MCE, HY‐10259A, USA); ISO + Ang‐(1–7) + PD123319 + A779. ..

Construct:

Sterility:

Article Title: Integrated multi-omics and functional analyses identify the renin-angiotensin system dysregulation as a central driver of lumbar disc herniation
Article Snippet: Introduction: Lumbar disc herniation (LDH) involves inflammation and metabolic stress.. Tissue-specific renin-angiotensin-aldosterone system (RAAS) signaling may act as an upstream regulator of disc degeneration.. This study investigates RAAS dysregulation as a central driver of LDH and its contribution to inflammation, metabolic reprogramming, and disc injury.

Saline:

Article Title: Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor
Article Snippet: .. After 7 days' acclimatization, animals were randomized (blinded assessment) into five groups ( n = 6 per group) receiving daily Subcutaneous injection for 7 days [ , , ]:Ctrl: saline (Sanlian, Harbin, China); ISO: isoproterenol 5 mg/kg/day (Solarbio, II0200, Beijing, China; dissolved in DMSO); ISO + Ang‐(1–7): Ang‐(1–7) 576 μg/kg/day (MCE, HY‐12403, USA; in distilled water); ISO + Ang‐(1–7) + A‐779: A‐7791148 μg/kg/day (MCE, HY‐P0216, USA); ISO + Ang‐(1–7) + PD123319 : PD123319 5 mg/kg/day (MCE, HY‐10259A, USA); ISO + Ang‐(1–7) + PD123319 + A779. ..

Image Search Results

Physical and chemical properties and biosafety assessment of Ang‐(1–7). (A) Key molecular properties: molecular weight (MW), net charge, isoelectric point (pI), hydrophobicity (GRAVY index), and aromaticity. (B, C) Topological structure predicted by Deep TMHMM, showing a spherical soluble conformation (no transmembrane helices) and predicted functional sites (red‐intracellular; blue‐extracellular). (D) Hemolytic activity ( n = 6). (E) Cytotoxicity assessment in H9c2, HepG2, and NRK‐52E cell lines ( n = 6). Cell viability was determined using the Cell Counting Kit‐8 (CCK‐8) assay. The data is expressed as an mean ± standard deviation (SD).

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Physical and chemical properties and biosafety assessment of Ang‐(1–7). (A) Key molecular properties: molecular weight (MW), net charge, isoelectric point (pI), hydrophobicity (GRAVY index), and aromaticity. (B, C) Topological structure predicted by Deep TMHMM, showing a spherical soluble conformation (no transmembrane helices) and predicted functional sites (red‐intracellular; blue‐extracellular). (D) Hemolytic activity ( n = 6). (E) Cytotoxicity assessment in H9c2, HepG2, and NRK‐52E cell lines ( n = 6). Cell viability was determined using the Cell Counting Kit‐8 (CCK‐8) assay. The data is expressed as an mean ± standard deviation (SD).

Article Snippet: After 7 days' acclimatization, animals were randomized (blinded assessment) into five groups ( n = 6 per group) receiving daily Subcutaneous injection for 7 days [ , , ]:Ctrl: saline (Sanlian, Harbin, China); ISO: isoproterenol 5 mg/kg/day (Solarbio, II0200, Beijing, China; dissolved in DMSO); ISO + Ang‐(1–7): Ang‐(1–7) 576 μg/kg/day (MCE, HY‐12403, USA; in distilled water); ISO + Ang‐(1–7) + A‐779: A‐7791148 μg/kg/day (MCE, HY‐P0216, USA); ISO + Ang‐(1–7) + PD123319 : PD123319 5 mg/kg/day (MCE, HY‐10259A, USA); ISO + Ang‐(1–7) + PD123319 + A779.

Techniques: Molecular Weight, Functional Assay, Activity Assay, Cell Counting, CCK-8 Assay, Standard Deviation

$Effects of Ang‐(1–7) on isoproterenol (ISO)‐induced cardiac hypertrophy and fibrosis. (A) HE staining and Masson staining of myocardial sections (scale bar = 20 μm). (B, C) Quantitative analysis of myocardial cell cross‐sectional area and collagen volume fraction. (D, E) Macroscopic morphology and cross‐sectional observation of the heart, with measurement of heart weight/body weight ratio (HW/BW) (scale bar = 2 mm). (F) Western blot analysis of ANP, BNP, and β‐MHC expression. (G–I) Quantitative analysis of band intensity normalized to GAPDH. The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM+A + I, A‐779 + Ang‐(1–7) + ISO; AntA+A + I, PD123319 + Ang‐(1–7) + ISO. *** p < 0.001 versus Ctrl; ### p < 0.001 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.$

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Effects of Ang‐(1–7) on isoproterenol (ISO)‐induced cardiac hypertrophy and fibrosis. (A) HE staining and Masson staining of myocardial sections (scale bar = 20 μm). (B, C) Quantitative analysis of myocardial cell cross‐sectional area and collagen volume fraction. (D, E) Macroscopic morphology and cross‐sectional observation of the heart, with measurement of heart weight/body weight ratio (HW/BW) (scale bar = 2 mm). (F) Western blot analysis of ANP, BNP, and β‐MHC expression. (G–I) Quantitative analysis of band intensity normalized to GAPDH. The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM+A + I, A‐779 + Ang‐(1–7) + ISO; AntA+A + I, PD123319 + Ang‐(1–7) + ISO. *** p < 0.001 versus Ctrl; ### p < 0.001 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.

Techniques: Staining, Western Blot, Expressing, Standard Deviation

$Ang‐(1–7) improves ISO‐induced ventricular remodeling and dysfunction via MasR and AT 2 R. (A) Representative M‐mode echocardiograms from each group (scale bar = 2 mm). (B, C) Quantification of left ventricular internal diameters at systole (LVIDs) and diastole (LVIDd). (D, E) Left ventricular ejection fraction (LVEF%) and fractional shortening (LVFS%). (F, G) Left ventricular posterior wall thickness at systole (LVPWs) and diastole (LVPWd). (H) Representative immunofluorescence images of cardiomyocytes (green, α‐actinin; blue, nuclei; scale bar = 10 μm). (I) Relative mRNA expression of ANP, BNP, and β‐MHC ( n = 6). The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; AntA + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO. *** p < 0.001, ** p < 0.01 versus Ctrl; ### p < 0.001, ## p < 0.01 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO, & p < 0.05 versus ISO.$

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Ang‐(1–7) improves ISO‐induced ventricular remodeling and dysfunction via MasR and AT 2 R. (A) Representative M‐mode echocardiograms from each group (scale bar = 2 mm). (B, C) Quantification of left ventricular internal diameters at systole (LVIDs) and diastole (LVIDd). (D, E) Left ventricular ejection fraction (LVEF%) and fractional shortening (LVFS%). (F, G) Left ventricular posterior wall thickness at systole (LVPWs) and diastole (LVPWd). (H) Representative immunofluorescence images of cardiomyocytes (green, α‐actinin; blue, nuclei; scale bar = 10 μm). (I) Relative mRNA expression of ANP, BNP, and β‐MHC ( n = 6). The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; AntA + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO. *** p < 0.001, ** p < 0.01 versus Ctrl; ### p < 0.001, ## p < 0.01 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO, & p < 0.05 versus ISO.

Techniques: Immunofluorescence, Expressing, Standard Deviation

Ang‐(1–7) regulates the expression of MasR and AT 2 R in H9c2 cardiomyocytes and exhibits cross‐inhibition with receptor antagonists. (A) Immunofluorescence images and immunofluorescence intensity of MasR (green), AT 2 R (red), and DAPI (blue) in H9c2 cells from different treatment groups, reflecting receptor expression levels (scale bar = 80 μm) ( n = 5). (B) Shows the expression of AT 2 R and MasR mRNA in H9c2 cells ( n = 6). (C) Analyzes MasR expression and relative thermal stability in cardiomyocytes at different temperatures (37°C–58°C). The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; AntA + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO. *** p < 0.001, * p < 0.05 versus Ctrl; #### p < 0.0001, ### p < 0.001 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Ang‐(1–7) regulates the expression of MasR and AT 2 R in H9c2 cardiomyocytes and exhibits cross‐inhibition with receptor antagonists. (A) Immunofluorescence images and immunofluorescence intensity of MasR (green), AT 2 R (red), and DAPI (blue) in H9c2 cells from different treatment groups, reflecting receptor expression levels (scale bar = 80 μm) ( n = 5). (B) Shows the expression of AT 2 R and MasR mRNA in H9c2 cells ( n = 6). (C) Analyzes MasR expression and relative thermal stability in cardiomyocytes at different temperatures (37°C–58°C). The data is expressed as an mean ± standard deviation (SD) ( n = 5). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; AntA + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO. *** p < 0.001, * p < 0.05 versus Ctrl; #### p < 0.0001, ### p < 0.001 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.

Techniques: Expressing, Inhibition, Immunofluorescence, Standard Deviation

Ang‐(1–7) regulates the expression of MasR and AT 2 R and their heterodimer formation. (A) Immunofluorescence staining images of MasR (green), AT 2 R (red), and DAPI (blue) in myocardial tissue from mice in each treatment group. Arrows indicate the localization of receptors in the myocardium (scale bar = 20 μm) ( n = 5). (B) Protein expression and quantitative analysis of MasR and AT 2 R in myocardial tissue ( n = 6). (C) Molecular docking simulations showing the interactions between MasR and AT 2 R, as well as between Ang‐(1–7) and the receptors, along with the binding energies (ΔG) for each interaction. (D) Immunoprecipitation (Co‐IP): Interaction between MasR and AT 2 R in cardiac muscle tissue. The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO. * p < 0.05 versus Ctrl; ### p < 0.001 versus ISO; &&& p < 0.001, & p < 0.05 versus Ang‐(1–7) + ISO.

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Ang‐(1–7) regulates the expression of MasR and AT 2 R and their heterodimer formation. (A) Immunofluorescence staining images of MasR (green), AT 2 R (red), and DAPI (blue) in myocardial tissue from mice in each treatment group. Arrows indicate the localization of receptors in the myocardium (scale bar = 20 μm) ( n = 5). (B) Protein expression and quantitative analysis of MasR and AT 2 R in myocardial tissue ( n = 6). (C) Molecular docking simulations showing the interactions between MasR and AT 2 R, as well as between Ang‐(1–7) and the receptors, along with the binding energies (ΔG) for each interaction. (D) Immunoprecipitation (Co‐IP): Interaction between MasR and AT 2 R in cardiac muscle tissue. The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO. * p < 0.05 versus Ctrl; ### p < 0.001 versus ISO; &&& p < 0.001, & p < 0.05 versus Ang‐(1–7) + ISO.

Techniques: Expressing, Immunofluorescence, Staining, Binding Assay, Immunoprecipitation, Co-Immunoprecipitation Assay, Standard Deviation

Ang‐(1–7) attenuates ISO‐induced excessive autophagy and apoptosis in vivo by regulating MasR and AT 2 R. (A) Transmission electron microscopy (TEM) images showing autophagosomes, lysosomes, and damaged mitochondria in cardiomyocytes; quantification of damaged mitochondria is shown (scale bar = 5 μm, 2 μm n = 4). (B) Western blot analysis of autophagy‐related proteins LC3‐II/I, Beclin1, and P62 ( n = 5). (C) Western blot analysis of apoptosis‐related proteins Bcl‐2, Bax, and cleaved caspase‐3 ( n = 5). (D, E) Quantitative densitometry analysis of autophagy‐ and apoptosis‐related proteins normalized to GAPDH. The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO. *** p < 0.001 versus Ctrl; ### p < 0.001, # p < 0.05 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Ang‐(1–7) attenuates ISO‐induced excessive autophagy and apoptosis in vivo by regulating MasR and AT 2 R. (A) Transmission electron microscopy (TEM) images showing autophagosomes, lysosomes, and damaged mitochondria in cardiomyocytes; quantification of damaged mitochondria is shown (scale bar = 5 μm, 2 μm n = 4). (B) Western blot analysis of autophagy‐related proteins LC3‐II/I, Beclin1, and P62 ( n = 5). (C) Western blot analysis of apoptosis‐related proteins Bcl‐2, Bax, and cleaved caspase‐3 ( n = 5). (D, E) Quantitative densitometry analysis of autophagy‐ and apoptosis‐related proteins normalized to GAPDH. The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO. *** p < 0.001 versus Ctrl; ### p < 0.001, # p < 0.05 versus ISO; &&& p < 0.001, && p < 0.01, & p < 0.05 versus Ang‐(1–7) + ISO.

Techniques: In Vivo, Transmission Assay, Electron Microscopy, Western Blot, Standard Deviation

Ang‐(1–7) regulates autophagic flux and apoptosis in H9c2 cardiomyocytes through MasR and AT 2 R. (A) Representative images of TUNEL immunofluorescence staining (green fluorescence labels apoptotic cells) and Hoechst nuclear staining (blue) ( n = 6), with the Merge panel showing their overlay. (B) Western blot analysis of apoptosis related proteins (Bax, Bcl 2 , Cleaved caspase‐3) expression levels, with GAPDH as the internal control protein ( n = 3). (C) Western blot analysis of autophagy‐related proteins (LC3‐II, Beclin1, P62) expression levels, with GAPDH as the internal control protein ( n = 3). The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO.

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Figure Lengend Snippet: Ang‐(1–7) regulates autophagic flux and apoptosis in H9c2 cardiomyocytes through MasR and AT 2 R. (A) Representative images of TUNEL immunofluorescence staining (green fluorescence labels apoptotic cells) and Hoechst nuclear staining (blue) ( n = 6), with the Merge panel showing their overlay. (B) Western blot analysis of apoptosis related proteins (Bax, Bcl 2 , Cleaved caspase‐3) expression levels, with GAPDH as the internal control protein ( n = 3). (C) Western blot analysis of autophagy‐related proteins (LC3‐II, Beclin1, P62) expression levels, with GAPDH as the internal control protein ( n = 3). The data is expressed as an mean ± standard deviation (SD). A + I, Ang‐(1–7) + ISO; AntM + A + I, A‐779 + Ang‐(1–7) + ISO; Ant A + A + I, PD123319 + Ang‐(1–7) + ISO; AntM + AntA + A + I, A‐779 + PD123319 + Ang‐(1–7) + ISO.

Techniques: TUNEL Assay, Immunofluorescence, Staining, Fluorescence, Western Blot, Expressing, Control, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: Molecular Weight, Functional Assay, Activity Assay, Cell Counting, CCK-8 Assay, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: Staining, Western Blot, Expressing, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: Immunofluorescence, Expressing, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: Expressing, Inhibition, Immunofluorescence, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: Expressing, Immunofluorescence, Staining, Binding Assay, Immunoprecipitation, Co-Immunoprecipitation Assay, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: In Vivo, Transmission Assay, Electron Microscopy, Western Blot, Standard Deviation

Journal: Acta Physiologica (Oxford, England)

doi: 10.1111/apha.70200

Techniques: TUNEL Assay, Immunofluorescence, Staining, Fluorescence, Western Blot, Expressing, Control, Standard Deviation

Ang II treatment increases the expression of MyD88 in mouse heart tissues. C57BL/6 mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Protein levels of MyD88 in heart tissues from normal (Ctrl) and Ang II‐treated (Ang II) mice were measured using Western blot analysis. GAPDH was used as the loading control. Representative Western blot images (left panel) and densitometric quantifications (right panel) are shown. (B–D) The cellular distribution of MyD88 in heart tissues from normal and Ang II‐infused mice was determined using the immunofluorescence assay. Representative immunofluorescence images of MyD88 (red) in α‐actinin staining‐positive cardiomyocytes (green), vimentin staining‐positive fibroblasts (green), and CD68 staining‐positive macrophages (green) are shown. Sections were counterstained with DAPI (blue). Scale bar = 20 μm. Statistical data were presented as mean ± SEM, n = 5; ** p < 0.01 compared to the control group (Ctrl).

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: Ang II treatment increases the expression of MyD88 in mouse heart tissues. C57BL/6 mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Protein levels of MyD88 in heart tissues from normal (Ctrl) and Ang II‐treated (Ang II) mice were measured using Western blot analysis. GAPDH was used as the loading control. Representative Western blot images (left panel) and densitometric quantifications (right panel) are shown. (B–D) The cellular distribution of MyD88 in heart tissues from normal and Ang II‐infused mice was determined using the immunofluorescence assay. Representative immunofluorescence images of MyD88 (red) in α‐actinin staining‐positive cardiomyocytes (green), vimentin staining‐positive fibroblasts (green), and CD68 staining‐positive macrophages (green) are shown. Sections were counterstained with DAPI (blue). Scale bar = 20 μm. Statistical data were presented as mean ± SEM, n = 5; ** p < 0.01 compared to the control group (Ctrl).

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: Expressing, Saline, Western Blot, Control, Immunofluorescence, Staining

Cardiac‐specific knockout of MyD88 exhibits no significant therapeutic effect on Ang II‐induced cardiac hypertrophy. MyD88 f/f and MyD88 f/f Myh6‐Cre mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H) and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 6; ** p < 0.01 compared to the MyD88 f/f group; ns = not significant, compared to the MyD88 f/f + Ang II group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: Cardiac‐specific knockout of MyD88 exhibits no significant therapeutic effect on Ang II‐induced cardiac hypertrophy. MyD88 f/f and MyD88 f/f Myh6‐Cre mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H) and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 6; ** p < 0.01 compared to the MyD88 f/f group; ns = not significant, compared to the MyD88 f/f + Ang II group.

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: Knock-Out, Saline, Staining, Quantitative RT-PCR

Macrophage‐specific knockout of MyD88 attenuates Ang II‐induced cardiac hypertrophy. MyD88 f/f and MyD88 f/f Lyz2‐Cre mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H), and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 5; * p < 0.05; ** p < 0.01, compared to the MyD88 f/f group; # p < 0.05 compared to the MyD88 f/f + Ang II group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: Macrophage‐specific knockout of MyD88 attenuates Ang II‐induced cardiac hypertrophy. MyD88 f/f and MyD88 f/f Lyz2‐Cre mice were continuously challenged with Ang II (1 μg/kg/min) or normal saline using micro‐osmotic pumps for 4 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H), and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 5; * p < 0.05; ** p < 0.01, compared to the MyD88 f/f group; # p < 0.05 compared to the MyD88 f/f + Ang II group.

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: Knock-Out, Saline, Staining, Quantitative RT-PCR

MyD88 inhibitor ameliorates Ang II‐induced cardiac hypertrophy in vivo. C57BL/6 mice were continuously challenged with Ang II (1 μg/kg/min) using micro‐osmotic pumps for 4 weeks. Three weeks after Ang II infusion, mice were administered with MyD88 inhibitor, LM8 (5 or 10 mg/kg), or vehicle control (CMC‐Na) via oral gavage daily for 2 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H) and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 6; *** p < 0.001, compared to the Ctrl group; # p < 0.05; ## p < 0.01; ### p < 0.001, compared to the Ang II group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: MyD88 inhibitor ameliorates Ang II‐induced cardiac hypertrophy in vivo. C57BL/6 mice were continuously challenged with Ang II (1 μg/kg/min) using micro‐osmotic pumps for 4 weeks. Three weeks after Ang II infusion, mice were administered with MyD88 inhibitor, LM8 (5 or 10 mg/kg), or vehicle control (CMC‐Na) via oral gavage daily for 2 weeks. (A) Representative images of heart tissues. (B) Haematoxylin & Eosin staining showing myocardial fibre arrangements in heart tissues [scale bar = 30 μm]. (C) WGA‐FITC staining showing the cross‐sectional area of cardiomyocytes in heart tissues [scale bar = 20 μm]. (D) Masson's staining showing the interstitial fibrotic area in heart tissues [scale bar = 30 μm]. (E) Sirius Red staining showing the heart tissue fibres [scale bar = 30 μm]. (F) Anti‐F4/80 staining showing macrophage infiltration in heart tissues [scale bar = 30 μm]. (G–I) RT‐qPCR analysis of Il1b (G), Il6 (H) and Tnfa (I) in heart tissues. Data were presented as mean ± SEM, n = 6; *** p < 0.001, compared to the Ctrl group; # p < 0.05; ## p < 0.01; ### p < 0.001, compared to the Ang II group.

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: In Vivo, Control, Staining, Quantitative RT-PCR

MyD88 mediates Ang II‐induced macrophage infiltration via regulating chemokine secretion. (A) RT‐qPCR analysis of inflammatory chemokines and cytokines in heart tissues from MyD88 cardiac‐specific knockout (upper panel) and MyD88 macrophage‐specific knockout mice (lower panel) with or without Ang II treatment. (B) RT‐qPCR validation of Cxcl1 and Ccl2 mRNA levels in heart tissues of Ang II‐challenged mice with or without LM8 treatment. (C) RT‐qPCR analysis of Cxcl1 and Ccl2 mRNA levels in MyD88‐deficient macrophages challenged with 1 μM Ang II for 6 h. (D) Macrophage adhesion experiments. Macrophages derived from MyD88 f/f Lyz2‐Cre mice were incubated with CFSE for 30 min, followed by stimulation with 1 μM Ang II for 6 h. The stimulated MyD88‐deficient macrophages were added to the cultured H9c2 cells for 4 h. The non‐attached macrophages were washed three times with PBS. The attached macrophages were measured by detecting CFSE immunofluorescence [scale bar = 100 μm]. (E) Representative Western blot images of the NF‐κB pathway in cardiac tissues from MyD88 f/f Lyz2‐Cre mice infused with Ang II. The right panel shows the densitometric quantifications. (F) Representative Western blot images of the NF‐κB pathway in cardiac tissues from LM8‐treated C57BL/6 mice infused with Ang II. The right panel shows the densitometric quantifications. Statistical data were presented as mean ± SEM, n = 5–6 for in vivo data, n = 3–5 for in vitro data; * p < 0.05; ** p < 0.01, compared to the Ctrl group; # p < 0.05 compared to the Ang II‐treated group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: MyD88 mediates Ang II‐induced macrophage infiltration via regulating chemokine secretion. (A) RT‐qPCR analysis of inflammatory chemokines and cytokines in heart tissues from MyD88 cardiac‐specific knockout (upper panel) and MyD88 macrophage‐specific knockout mice (lower panel) with or without Ang II treatment. (B) RT‐qPCR validation of Cxcl1 and Ccl2 mRNA levels in heart tissues of Ang II‐challenged mice with or without LM8 treatment. (C) RT‐qPCR analysis of Cxcl1 and Ccl2 mRNA levels in MyD88‐deficient macrophages challenged with 1 μM Ang II for 6 h. (D) Macrophage adhesion experiments. Macrophages derived from MyD88 f/f Lyz2‐Cre mice were incubated with CFSE for 30 min, followed by stimulation with 1 μM Ang II for 6 h. The stimulated MyD88‐deficient macrophages were added to the cultured H9c2 cells for 4 h. The non‐attached macrophages were washed three times with PBS. The attached macrophages were measured by detecting CFSE immunofluorescence [scale bar = 100 μm]. (E) Representative Western blot images of the NF‐κB pathway in cardiac tissues from MyD88 f/f Lyz2‐Cre mice infused with Ang II. The right panel shows the densitometric quantifications. (F) Representative Western blot images of the NF‐κB pathway in cardiac tissues from LM8‐treated C57BL/6 mice infused with Ang II. The right panel shows the densitometric quantifications. Statistical data were presented as mean ± SEM, n = 5–6 for in vivo data, n = 3–5 for in vitro data; * p < 0.05; ** p < 0.01, compared to the Ctrl group; # p < 0.05 compared to the Ang II‐treated group.

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: Quantitative RT-PCR, Knock-Out, Biomarker Discovery, Derivative Assay, Incubation, Cell Culture, Immunofluorescence, Western Blot, In Vivo, In Vitro

Conditioned medium from MyD88‐deficient macrophages fails to induce cardiomyocyte hypertrophy. (a) Schematic illustration of the experimental design of the conditioned medium study. Primary macrophages derived from MyD88 f/f and MyD88 f/f Lyz2‐Cre mice were treated with LPS (50 μg/mL) or PBS for 24 h. The cell culture medium was collected as the conditioned medium. H9c2 cells were treated with different conditioned medium for 24 h. (b) The protein levels of β‐Myhc, Col‐1, and TGF‐β in primary cardiomyocytes were evaluated using Western blot analysis. Representative images (upper panel) and the densitometric quantifications (lower panel) are shown. (c) Representative images of Rhodamine phalloidin staining in H9c2 cells [scale bar = 30 μm] (left panel). The statistical quantification of cellular hypertrophy was shown (right panel). (d) Schematic demonstrating mechanisms involved in Myeloid MyD88 mediates macrophage infiltration and activation in Ang II‐induced cardiac hypertrophy. Statistical data were presented as mean ± SEM, n = 3 for in vitro data; * p < 0.05 compared to group 1; # p < 0.05 compared to group 2.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II ‐Induced Cardiac Hypertrophy

doi: 10.1111/jcmm.70733

Figure Lengend Snippet: Conditioned medium from MyD88‐deficient macrophages fails to induce cardiomyocyte hypertrophy. (a) Schematic illustration of the experimental design of the conditioned medium study. Primary macrophages derived from MyD88 f/f and MyD88 f/f Lyz2‐Cre mice were treated with LPS (50 μg/mL) or PBS for 24 h. The cell culture medium was collected as the conditioned medium. H9c2 cells were treated with different conditioned medium for 24 h. (b) The protein levels of β‐Myhc, Col‐1, and TGF‐β in primary cardiomyocytes were evaluated using Western blot analysis. Representative images (upper panel) and the densitometric quantifications (lower panel) are shown. (c) Representative images of Rhodamine phalloidin staining in H9c2 cells [scale bar = 30 μm] (left panel). The statistical quantification of cellular hypertrophy was shown (right panel). (d) Schematic demonstrating mechanisms involved in Myeloid MyD88 mediates macrophage infiltration and activation in Ang II‐induced cardiac hypertrophy. Statistical data were presented as mean ± SEM, n = 3 for in vitro data; * p < 0.05 compared to group 1; # p < 0.05 compared to group 2.

Article Snippet: The Ang II ELISA kit (#E‐EL‐H5518c) was purchased from Elabscience (Wuhan, China).

Techniques: Derivative Assay, Cell Culture, Western Blot, Staining, Activation Assay, In Vitro

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