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
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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 .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_8652/pmc13098652/pmc13098652__atv-46-e323681-g006.jpg)