Abstract
Aims of the Study
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.
Acknowledgements
We thank Lishui University for providing the PhD research startup fund.
Statement of ethics
All procedures were approved by the Animal Research Ethics Board of the Lishui University and all experiments were performed in accordance with relevant guidelines and regulations.
Declaration of interest
No conflict of interest to disclose. Fang Dong and Jun Zhang contributed equally to this work. JZ initiated and designed the project, analyzed data and wrote the article. JZ and FD performed all experiments together.