期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 280, 期 2, 页码 H746-H755出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.280.2.H746
关键词
transient receptor potential gene; pulmonary hypertension; pulmonary artery smooth muscle cells
资金
- NHLBI NIH HHS [HL-64945, HL-54043] Funding Source: Medline
A rise in cytosolic Ca2+ concentration ([Ca2+](cyt)) due to Ca2+ release from intracellular Ca2+ stores and Ca2+ influx through plasmalemmal Ca2+ channels plays a critical role in mitogen-mediated cell growth. Depletion of intracellular Ca2+ stores triggers capacitative Ca2+ entry (CCE), a mechanism involved in maintaining Ca2+ influx and refilling intracellular Ca2+ stores. Transient receptor potential (TRP) genes have been demonstrated to encode the store-operated Ca2+ channels that are activated by Ca2+ store depletion. In this study, we examined whether CCE, activity of store-operated Ca2+ channels, and human TRP1 (hTRP1) expression are essential in human pulmonary arterial smooth muscle cell (PASMC) proliferation. Chelation of extracellular Ca2+ and depletion of intracellularly stored Ca2+ inhibited PASMC growth in media containing serum and growth factors. Resting [Ca2+](cyt) as well as the increases in [Ca2+](cyt) due to Ca2+ release and CCE were all significantly greater in proliferating PASMC than in growth-arrested cells. Consistently, whole cell inward currents activated by depletion of intracellular Ca2+ stores and the mRNA level of hTRP1 were much greater in proliferating PASMC than in growth-arrested cells. These results suggest that elevated [Ca2+](cyt) and intracellularly stored [Ca2+] play an important role in pulmonary vascular smooth muscle cell growth. CCE, potentially via hTRP1-encoded Ca2+-permeable channels, may be an important mechanism required to maintain the elevated [Ca2+](cyt) and stored [Ca2+] in human PASMC during proliferation.
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