To investigate the effect of carboxyl terminus of Hsc70-interacting protein (CHIP) on pulmonary arterial smooth muscle cell (PASMC) proliferation and the underlying mechanism. Materials and Methods: PASMCs were harvested from distal PAs isolated from SD rat lungs and cultured. After CHIP overexpression, PASMCs were exposed to normoxia or hypoxia for 60 h. Then, PASMC proliferation, store-operated Ca2+ entry (SOCE), [Ca2+]i and the expression of TRPC1, TRPC4, and TRPC6 in PASMCs were measured. Results: CHIP overexpression promoted PASMC proliferation, SOCE, [Ca2+]i and the expression of TRPC1, TRPC4, and TRPC6. Conclusions: CHIP stimulates PASMC proliferation likely by targeting the TRPC1,4,6-SOCE-[Ca2+]i signaling pathway.
Keywords: CHIP; PASMCs; SOCE; TRPC; [Ca2+]i.