TGF-β1 inhibits the apoptosis of pulmonary arterial smooth muscle cells and contributes to pulmonary vascular medial thickening via the PI3K/Akt pathway.

Previous studies have highlighted that the transforming growth factor‑β1 (TGF‑β1) pathway may be activated by hypoxic conditions. TGF‑β1 also participates in the regulation of proliferation, differentiation, migration and apoptosis of various cell types. Furthermore, TGF‑β1 has been reported to participate in the regulation of the progression of pulmonary arterial hypertension (PAH). However, the effect of TGF‑β1 on pulmonary arterial smooth muscle cells (PASMCs) and the corresponding molecular mechanisms remain unclear. The present study aimed to determine whether TGF‑β1 protects against cell apoptosis in PASMCs, and identify the underlying molecular mechanisms. Western blotting, MTT and lactate dehydrogenase activity assays were performed, and the activity of caspase‑3 and caspase‑9 was detected in order to investigate the hypothesis. It was determined that TGF‑β1 may facilitate cell growth in a dose‑dependent manner in serum‑starved PASMCs. Furthermore, it was observed that apoptosis in serum‑starved PASMCs was inhibited by TGF‑β1 via regulation of the expression levels of mitochondrial membrane proteins. Additionally, the phosphatidylinositol 3‑kinase/protein kinase B (PI3K/Akt) pathway was found to be activated by TGF‑β1 in PASMCs, while the inhibition of PI3K/Akt signaling also prevented the apoptosis‑limiting effects of TGF‑β1. These observations suggest that TGF‑β1 protects PASMCs from apoptosis and contributes to pulmonary vascular medial thickening via the PI3K/Akt pathway.