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vegf inhibitor su5416  (MedChemExpress)


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    Structured Review

    MedChemExpress vegf inhibitor su5416
    A Schematic diagram of the <t>SU5416</t> combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.
    Vegf Inhibitor Su5416, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 79 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Super Enhancer-driven LncRNA UNC5B-AS1 Inhibits Inflammatory Phenotypic Transition in Smooth Muscle Cells via Lactylation Modification"

    Article Title: Super Enhancer-driven LncRNA UNC5B-AS1 Inhibits Inflammatory Phenotypic Transition in Smooth Muscle Cells via Lactylation Modification

    Journal: bioRxiv

    doi: 10.1101/2024.05.07.593065

    A Schematic diagram of the SU5416 combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.
    Figure Legend Snippet: A Schematic diagram of the SU5416 combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.

    Techniques Used: Expressing, Staining, Negative Control, Over Expression



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    A Schematic diagram of the <t>SU5416</t> combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.
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    A Schematic diagram of the <t>SU5416</t> combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.
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    Inhibition of RUNX1 in vivo prevents the development of Sugen/hypoxia-induced pulmonary hypertension (SuHx-PH) in rats. ( A ) Experimental protocol for prevention of SuHx-PH in rats shows administration of the RUNX1 inhibitor Ro5-3335 (Ro5) every other day for three times at the beginning of SuHx treatment. <t>SU5416:</t> VEGF receptor 2 antagonist Sugen 5416. ( B and C ) Right ventricular systolic pressure (RVSP) ( B ) and the Fulton’s index (right ventricle to left ventricle + septum, RV/LV+S ratio) ( C ) were measured 1 week after removal from 3 weeks of hypoxia (Hx). ( D – F ) Representative microscopic images of 100× magnification show immunohistochemical (IHC) staining in brown colour of α-smooth muscle actin (α-SMA) in the blood vessels from lungs of normoxia control (Nx Ctrl) rats ( D ), vehicle DMSO-treated SuHx rats ( E ), and 20 mg/kg Ro5-treated SuHx rats ( F ). ( G ) Muscularization of distal pulmonary vessels less than 50 µm in diameter was assessed by calculating the muscularization index defined as the total area of the vessel that stained positive for α-SMA divided by total cross-sectional area of the vessel. ( H – J ) Representative small blood vessels stained in brown colour of α-SMA, which are labelled with a red asterisk in ( D – F ), are shown in 600× magnification: ( H ) Nx Ctrl rats; ( I ) vehicle DMSO-treated SuHx rats; and ( J ) Ro5-treated SuHx rats. ** P < 0.01, *** P < 0.001, **** P < 0.0001, n.s.: not significant, ordinary one-way ANOVA with multiple comparisons, n = number of animals in each experimental group.
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    Endothelial glycocalyx impairment is involved in <t>SU5416-induced</t> rat emphysema model. Male Sprague-Dawley rats (~ 300 g) were treated with VEGF-R antagonist SU5416 (20 mg/kg) subcutaneously 3 times per week for 3 weeks. A Representative haematoxylin and eosin (H&E) staining images of airspace. Scale bar = 50 μm. Alveolar size was measured by mean linear intercept (MLI) (n = 5). B Cleaved caspase-3 antibody was used as the mark of cell apoptosis. Group data of cleaved caspase-3 positive cells per field (n = 5). Scale bar = 50 μm. C Representative immunofluorescence staining images of rat lung sections. Heparan sulfate and Chondroitin sulfate antibodies were used as glycocalyx specific antigens, and CD31 was used as the mark of endothelial cell. Nuclei were visualized with 4ʹ,6-diamidino-2-phenylindole (DAPI). Scale bar = 20 μm. Quantitative analysis of fluorescence intensity for heparan sulfate, chondroitin sulfate and syndecan-1 (n = 5). D ELISA analysis of blood and BALF samples (n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. n.s., not significant
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    Pretreatment with a VEGF pathway inhibitor prevented the formation of intersomitic vessels: The panels show representative images of a WISH assay performed with fli1 as an endothelial marker, at 36 hpf, in untreated ( A , C , E , G , I ) and treated embryos ( B , D , F , H , J ) with SUGEN 5416. Previously, some embryos were treated with snail derivatives via Method I and controls with fish water and 0.1% DMSO (see Materials and Methods,  and  ). Magnification of the trunk region (32×). Two replicates were performed ( n = 15). Ratios at the bottom-left part of each picture specify the number of embryos showing the same staining pattern, compared to the total number of embryos used for each experiment. The images were taken in lateral position at 32× magnification with a Zeiss Axiozoom V13 (Zeiss, Jena, Germany) microscope, equipped with a PlanNeoFluar Z 1×/0.25 FWD 56 mm lens and Zen Pro software.
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    Fsta regulates BMP signals to control vascular patterning. ( A – D ) Inhibition of VEGF or Notch signals by <t>SU5416</t> or DAPT treatment reduced the expression of fsta compared to DMSO-treated control. ( E – H ) Inhibition of BMP signals by DM or DMH1 treatment did not reduce the expression of fsta in embryos by in-situ hybridization and qPCR analysis. ( I ) Representative western blot assays showed the reduced phosphorylation of smad1 and ERK1/2 in (fli:fsta ) embryos. β-actin serves as loading controls. ( J ) The decreased expression of BMP regulated genes id1 , eve1 , msx1b and gata2 . qPCR data are presented as the mean ± S.D. *** refers to p < 0.0001 and ** refers to p < 0.001 by an unpaired Student’s t -test. Scale bar represents 200 μm in ( A – C , E – G ). ( K ) Schematic drawing shows the genetic regulation of fsta , isl2/nr2f1b , and multiply signals. Our data suggest that fsta functions in ISV growth and CVP patterning mediated by BMP signal pathways.
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    Fsta regulates BMP signals to control vascular patterning. ( A – D ) Inhibition of VEGF or Notch signals by <t>SU5416</t> or DAPT treatment reduced the expression of fsta compared to DMSO-treated control. ( E – H ) Inhibition of BMP signals by DM or DMH1 treatment did not reduce the expression of fsta in embryos by in-situ hybridization and qPCR analysis. ( I ) Representative western blot assays showed the reduced phosphorylation of smad1 and ERK1/2 in (fli:fsta ) embryos. β-actin serves as loading controls. ( J ) The decreased expression of BMP regulated genes id1 , eve1 , msx1b and gata2 . qPCR data are presented as the mean ± S.D. *** refers to p < 0.0001 and ** refers to p < 0.001 by an unpaired Student’s t -test. Scale bar represents 200 μm in ( A – C , E – G ). ( K ) Schematic drawing shows the genetic regulation of fsta , isl2/nr2f1b , and multiply signals. Our data suggest that fsta functions in ISV growth and CVP patterning mediated by BMP signal pathways.
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    Image Search Results


    A Schematic diagram of the SU5416 combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.

    Journal: bioRxiv

    Article Title: Super Enhancer-driven LncRNA UNC5B-AS1 Inhibits Inflammatory Phenotypic Transition in Smooth Muscle Cells via Lactylation Modification

    doi: 10.1101/2024.05.07.593065

    Figure Lengend Snippet: A Schematic diagram of the SU5416 combined with hypoxia-induced PH (SuHx) mice model. B Expression of UNC5B-AS1 conserved fragment (UA1CF) in mice lungs (n=8). C Right ventricle/left ventricle + septum (RV/LV+ Septum) in mice (n=8). D Representative waveform of right ventricular systolic pressure. E Representative right ventricular systolic pressure (RVSP) in mice (n=8). Pulmonary artery acceleration time (PAAT, F ), pulmonary artery velocity-time integral (PAVTI, G ), ejection fraction (EF, H ) in mice (n=8). I Representative images of Hematoxylin and Eosin staining (H&E) and Masson staining in mice lungs. Scale bars=50 μm. All data are presented as mean ± SEM. One-way ANOVA with Tukey post hoc test was used to compare multiple groups with equal variance, and Brown-Forsythe and Welch ANOVA with Tamhane T2 post hoc test was used to compare multiple groups with unequal variance. Nor, normoxia, SuHx, SU5416 combined with hypoxia, NC, Negative control and UA1CF, AAV5-UNC5B-AS1 conserved fragment overexpression.

    Article Snippet: In the Sugen hypoxia model, the mice were injected once per week with the VEGF inhibitor SU5416 (Med Chem Express, USA) at a concentration of 20 mg/kg.

    Techniques: Expressing, Staining, Negative Control, Over Expression

    Inhibition of RUNX1 in vivo prevents the development of Sugen/hypoxia-induced pulmonary hypertension (SuHx-PH) in rats. ( A ) Experimental protocol for prevention of SuHx-PH in rats shows administration of the RUNX1 inhibitor Ro5-3335 (Ro5) every other day for three times at the beginning of SuHx treatment. SU5416: VEGF receptor 2 antagonist Sugen 5416. ( B and C ) Right ventricular systolic pressure (RVSP) ( B ) and the Fulton’s index (right ventricle to left ventricle + septum, RV/LV+S ratio) ( C ) were measured 1 week after removal from 3 weeks of hypoxia (Hx). ( D – F ) Representative microscopic images of 100× magnification show immunohistochemical (IHC) staining in brown colour of α-smooth muscle actin (α-SMA) in the blood vessels from lungs of normoxia control (Nx Ctrl) rats ( D ), vehicle DMSO-treated SuHx rats ( E ), and 20 mg/kg Ro5-treated SuHx rats ( F ). ( G ) Muscularization of distal pulmonary vessels less than 50 µm in diameter was assessed by calculating the muscularization index defined as the total area of the vessel that stained positive for α-SMA divided by total cross-sectional area of the vessel. ( H – J ) Representative small blood vessels stained in brown colour of α-SMA, which are labelled with a red asterisk in ( D – F ), are shown in 600× magnification: ( H ) Nx Ctrl rats; ( I ) vehicle DMSO-treated SuHx rats; and ( J ) Ro5-treated SuHx rats. ** P < 0.01, *** P < 0.001, **** P < 0.0001, n.s.: not significant, ordinary one-way ANOVA with multiple comparisons, n = number of animals in each experimental group.

    Journal: Cardiovascular Research

    Article Title: Targeting RUNX1 as a novel treatment modality for pulmonary arterial hypertension

    doi: 10.1093/cvr/cvac001

    Figure Lengend Snippet: Inhibition of RUNX1 in vivo prevents the development of Sugen/hypoxia-induced pulmonary hypertension (SuHx-PH) in rats. ( A ) Experimental protocol for prevention of SuHx-PH in rats shows administration of the RUNX1 inhibitor Ro5-3335 (Ro5) every other day for three times at the beginning of SuHx treatment. SU5416: VEGF receptor 2 antagonist Sugen 5416. ( B and C ) Right ventricular systolic pressure (RVSP) ( B ) and the Fulton’s index (right ventricle to left ventricle + septum, RV/LV+S ratio) ( C ) were measured 1 week after removal from 3 weeks of hypoxia (Hx). ( D – F ) Representative microscopic images of 100× magnification show immunohistochemical (IHC) staining in brown colour of α-smooth muscle actin (α-SMA) in the blood vessels from lungs of normoxia control (Nx Ctrl) rats ( D ), vehicle DMSO-treated SuHx rats ( E ), and 20 mg/kg Ro5-treated SuHx rats ( F ). ( G ) Muscularization of distal pulmonary vessels less than 50 µm in diameter was assessed by calculating the muscularization index defined as the total area of the vessel that stained positive for α-SMA divided by total cross-sectional area of the vessel. ( H – J ) Representative small blood vessels stained in brown colour of α-SMA, which are labelled with a red asterisk in ( D – F ), are shown in 600× magnification: ( H ) Nx Ctrl rats; ( I ) vehicle DMSO-treated SuHx rats; and ( J ) Ro5-treated SuHx rats. ** P < 0.01, *** P < 0.001, **** P < 0.0001, n.s.: not significant, ordinary one-way ANOVA with multiple comparisons, n = number of animals in each experimental group.

    Article Snippet: Subsequent SuHx treatment consisted of 3 weekly subcutaneous injections of the Sugen VEGF receptor 2 inhibitor SU5416 at 20 mg/kg in 100 μL DMSO or vehicle alone.

    Techniques: Inhibition, In Vivo, Immunohistochemical staining, Immunohistochemistry, Control, Staining

    Endothelial glycocalyx impairment is involved in SU5416-induced rat emphysema model. Male Sprague-Dawley rats (~ 300 g) were treated with VEGF-R antagonist SU5416 (20 mg/kg) subcutaneously 3 times per week for 3 weeks. A Representative haematoxylin and eosin (H&E) staining images of airspace. Scale bar = 50 μm. Alveolar size was measured by mean linear intercept (MLI) (n = 5). B Cleaved caspase-3 antibody was used as the mark of cell apoptosis. Group data of cleaved caspase-3 positive cells per field (n = 5). Scale bar = 50 μm. C Representative immunofluorescence staining images of rat lung sections. Heparan sulfate and Chondroitin sulfate antibodies were used as glycocalyx specific antigens, and CD31 was used as the mark of endothelial cell. Nuclei were visualized with 4ʹ,6-diamidino-2-phenylindole (DAPI). Scale bar = 20 μm. Quantitative analysis of fluorescence intensity for heparan sulfate, chondroitin sulfate and syndecan-1 (n = 5). D ELISA analysis of blood and BALF samples (n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. n.s., not significant

    Journal: Respiratory Research

    Article Title: Fibroblast growth factor 10 attenuates chronic obstructive pulmonary disease by protecting against glycocalyx impairment and endothelial apoptosis

    doi: 10.1186/s12931-022-02193-5

    Figure Lengend Snippet: Endothelial glycocalyx impairment is involved in SU5416-induced rat emphysema model. Male Sprague-Dawley rats (~ 300 g) were treated with VEGF-R antagonist SU5416 (20 mg/kg) subcutaneously 3 times per week for 3 weeks. A Representative haematoxylin and eosin (H&E) staining images of airspace. Scale bar = 50 μm. Alveolar size was measured by mean linear intercept (MLI) (n = 5). B Cleaved caspase-3 antibody was used as the mark of cell apoptosis. Group data of cleaved caspase-3 positive cells per field (n = 5). Scale bar = 50 μm. C Representative immunofluorescence staining images of rat lung sections. Heparan sulfate and Chondroitin sulfate antibodies were used as glycocalyx specific antigens, and CD31 was used as the mark of endothelial cell. Nuclei were visualized with 4ʹ,6-diamidino-2-phenylindole (DAPI). Scale bar = 20 μm. Quantitative analysis of fluorescence intensity for heparan sulfate, chondroitin sulfate and syndecan-1 (n = 5). D ELISA analysis of blood and BALF samples (n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. n.s., not significant

    Article Snippet: Each cigarette smoke exposure duration lasted 1 h with an interval time between two exposures more than 4 h. (2) Rat emphysema model: To induce the emphysema formation in animals, the pan-vascular endothelial growth factor-receptor (VEGF-R) inhibitor SU5416 (20 mg/kg; MedChemExpress) suspended in solution (10% DMF mixed with 90% coin-oil; both obtained from MedChemExpress) was injected subcutaneously 3 times per week for 3 weeks. (3) Cigarette Smoke Extract (CSE)-induced mouse emphysema model: The emphysema mouse model was built according to the protocol of the previous study [ ].

    Techniques: Staining, Immunofluorescence, Fluorescence, Enzyme-linked Immunosorbent Assay

    Pretreatment with a VEGF pathway inhibitor prevented the formation of intersomitic vessels: The panels show representative images of a WISH assay performed with fli1 as an endothelial marker, at 36 hpf, in untreated ( A , C , E , G , I ) and treated embryos ( B , D , F , H , J ) with SUGEN 5416. Previously, some embryos were treated with snail derivatives via Method I and controls with fish water and 0.1% DMSO (see Materials and Methods,  and  ). Magnification of the trunk region (32×). Two replicates were performed ( n = 15). Ratios at the bottom-left part of each picture specify the number of embryos showing the same staining pattern, compared to the total number of embryos used for each experiment. The images were taken in lateral position at 32× magnification with a Zeiss Axiozoom V13 (Zeiss, Jena, Germany) microscope, equipped with a PlanNeoFluar Z 1×/0.25 FWD 56 mm lens and Zen Pro software.

    Journal: Current Issues in Molecular Biology

    Article Title: Pro-Angiogenetic Effects of Purified Extracts from Helix aspersa during Zebrafish Development

    doi: 10.3390/cimb44080232

    Figure Lengend Snippet: Pretreatment with a VEGF pathway inhibitor prevented the formation of intersomitic vessels: The panels show representative images of a WISH assay performed with fli1 as an endothelial marker, at 36 hpf, in untreated ( A , C , E , G , I ) and treated embryos ( B , D , F , H , J ) with SUGEN 5416. Previously, some embryos were treated with snail derivatives via Method I and controls with fish water and 0.1% DMSO (see Materials and Methods, and ). Magnification of the trunk region (32×). Two replicates were performed ( n = 15). Ratios at the bottom-left part of each picture specify the number of embryos showing the same staining pattern, compared to the total number of embryos used for each experiment. The images were taken in lateral position at 32× magnification with a Zeiss Axiozoom V13 (Zeiss, Jena, Germany) microscope, equipped with a PlanNeoFluar Z 1×/0.25 FWD 56 mm lens and Zen Pro software.

    Article Snippet: Zebrafish embryos were then treated at 4 hpf with the snail derivatives LH, LM, LH3, and LM2, and then at 15 hpf with the VEGF inhibitor SU5416 (Sunitinib, Merck KGaA, Darmstadt, Germany) at a final concentration of 5 μg/mL in fish water and incubated in 3 cm diameter well-plates.

    Techniques: Marker, Staining, Microscopy, Software

    Fsta regulates BMP signals to control vascular patterning. ( A – D ) Inhibition of VEGF or Notch signals by SU5416 or DAPT treatment reduced the expression of fsta compared to DMSO-treated control. ( E – H ) Inhibition of BMP signals by DM or DMH1 treatment did not reduce the expression of fsta in embryos by in-situ hybridization and qPCR analysis. ( I ) Representative western blot assays showed the reduced phosphorylation of smad1 and ERK1/2 in (fli:fsta ) embryos. β-actin serves as loading controls. ( J ) The decreased expression of BMP regulated genes id1 , eve1 , msx1b and gata2 . qPCR data are presented as the mean ± S.D. *** refers to p < 0.0001 and ** refers to p < 0.001 by an unpaired Student’s t -test. Scale bar represents 200 μm in ( A – C , E – G ). ( K ) Schematic drawing shows the genetic regulation of fsta , isl2/nr2f1b , and multiply signals. Our data suggest that fsta functions in ISV growth and CVP patterning mediated by BMP signal pathways.

    Journal: Biomedicines

    Article Title: Identification of Novel Vascular Genes Downstream of Islet2 and Nr2f1b Transcription Factors

    doi: 10.3390/biomedicines10061261

    Figure Lengend Snippet: Fsta regulates BMP signals to control vascular patterning. ( A – D ) Inhibition of VEGF or Notch signals by SU5416 or DAPT treatment reduced the expression of fsta compared to DMSO-treated control. ( E – H ) Inhibition of BMP signals by DM or DMH1 treatment did not reduce the expression of fsta in embryos by in-situ hybridization and qPCR analysis. ( I ) Representative western blot assays showed the reduced phosphorylation of smad1 and ERK1/2 in (fli:fsta ) embryos. β-actin serves as loading controls. ( J ) The decreased expression of BMP regulated genes id1 , eve1 , msx1b and gata2 . qPCR data are presented as the mean ± S.D. *** refers to p < 0.0001 and ** refers to p < 0.001 by an unpaired Student’s t -test. Scale bar represents 200 μm in ( A – C , E – G ). ( K ) Schematic drawing shows the genetic regulation of fsta , isl2/nr2f1b , and multiply signals. Our data suggest that fsta functions in ISV growth and CVP patterning mediated by BMP signal pathways.

    Article Snippet: To investigate signal pathways, the embryos were treated with 15 μM of the VEGF inhibitor SU5416 (Calbiochem, Nottingham, UK) and 75 μM of the Notch signal inhibitor DAPT (Sigma) at a working concentration in E3 fish water at 6 hpf.

    Techniques: Control, Inhibition, Expressing, In Situ Hybridization, Western Blot, Phospho-proteomics