关键词: 肺动脉平滑肌细胞, 瞬时感受器电位香草酸受体1, 钙库操控性通道

Abstract:

Objective To investigate the role of transient potential vanilloid receptor 1(TRPV1) channels on cytosolic Ca²⁺ concentration(340 nm/380 nm ratio of the fluorescence image) of hypoxic human pulmonary artery smooth muscle cells(HPASMCs) and its possible signal pathway. Methods 4',6-diamidino-2-phenylindole(DAPI) staining and flow cytometry were used to detect the proliferation of HPASMCs under normoxia or hypoxia (3％O₂, 72 h) conditions. Cytosolic Ca²⁺ concentration(［Ca²⁺］cyt) was measured with a dynamic digital imaging system. Results The capability of HPASMCs proliferation significantly increased under hypoxic condition. Capsazepine(a TRPV1 channel inhibitor) could inhibit the HPASMCs proliferation. Hypoxia markedly increased resting cytosolic Ca²⁺ concentration and enhanced cyclopiazonic acid-induced capacitative Ca²⁺ entry(CCE) in HPASMCs. Capsazepine(10 μM) decreased CCE under hypoxia condition, but there was no effect on normoxia cultured group. Conclusion These results suggest that TRPV1 may be a critical pathway or mediator in hypoxia-induced increase of cytosolic Ca²⁺ concentration, CCE and the proliferation of HPASMCs.

Key words: pulmonary arterial smooth muscle cells, transient potential vanilloid receptor 1, store-operated calcium channels