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ATCC human pulmonary artery endothelial cells
Human Pulmonary Artery Endothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Human Pulmonary Artery Endothelial Cells, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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PromoCell human pulmonary artery ecs
In vivo activin A inhibition improves <t>pulmonary</t> hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary <t>artery</t> muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung <t>ECs</t> isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .
Human Pulmonary Artery Ecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+pulmonary+artery+endothelial+cells/pmc13098652-17-0-7?v=PromoCell
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ATCC human primary pulmonary artery endothelial cells
In vivo activin A inhibition improves <t>pulmonary</t> hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary <t>artery</t> muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung <t>ECs</t> isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .
Human Primary Pulmonary Artery Endothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+pulmonary+artery+endothelial+cells/pm41892283-66-4-11?v=ATCC
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ATCC pulmonary artery smooth muscle cells
In vivo activin A inhibition improves <t>pulmonary</t> hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary <t>artery</t> muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung <t>ECs</t> isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .
Pulmonary Artery Smooth Muscle Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Procell Inc human pulmonary arterial endothelial cells hpaecs
In vivo activin A inhibition improves <t>pulmonary</t> hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary <t>artery</t> muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung <t>ECs</t> isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .
Human Pulmonary Arterial Endothelial Cells Hpaecs, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vivo activin A inhibition improves <t>pulmonary</t> hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary <t>artery</t> muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung <t>ECs</t> isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .
Hpaecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vivo activin A inhibition improves pulmonary hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary artery muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung ECs isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: In vivo activin A inhibition improves pulmonary hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary artery muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung ECs isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .

Article Snippet: Human pulmonary artery ECs (PAECs; no. C-12241; PromoCell) and pulmonary artery smooth muscle cells (PASMCs; no. C-12521; PromoCell) were cultured in HuMedia-EG2 (Kurabo) and smooth muscle cells growth medium 2 (PromoCell), respectively, at 37 °C and 5% CO 2 .

Techniques: In Vivo, Inhibition, Transgenic Assay, Staining, Marker, Expressing, Isolation