期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 453, 期 1, 页码 101-105出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2014.09.063
关键词
ARDS; ATP; Ca2+ signaling; Idiopathic pulmonary fibrosis; Mechanical stress; Mechanotransduction
资金
- Ministry of Education, Culture, Sports, Science and Technology of Japan [25461188, 25860209]
- Grants-in-Aid for Scientific Research [25860209, 26220203, 24590274, 25461188] Funding Source: KAKEN
One cause of progressive pulmonary fibrosis is dysregulated wound healing after lung inflammation or damage in patients with idiopathic pulmonary fibrosis and severe acute respiratory distress syndrome. The mechanical forces are considered to regulate pulmonary fibrosis via activation of lung fibroblasts. In this study, the effects of mechanical stretch on the intracellular Ca2+ concentration ([Ca2+](i)) and ATP release were investigated in primary human lung fibroblasts. Uniaxial stretch (10-30% in strain) was applied to fibroblasts cultured in a silicone chamber coated with type I collagen using a stretching apparatus. Following stretching and subsequent unloading, [Ca2+](i) transiently increased in a strain-dependent manner. Hypotonic stress, which causes plasma membrane stretching, also transiently increased the [Ca2+](i) The stretch-induced [Ca2+](i) elevation was attenuated in Ca2+-free solution. In contrast, the increase of [Ca2+](i) by a 20% stretch was not inhibited by the inhibitor of stretch-activated channels GsMTx-4, Gd3+, ruthenium red, or cytochalasin D. Cyclic stretching induced significant ATP releases from fibroblasts. However, the stretch-induced [Ca2+](i) elevation was not inhibited by ATP diphosphohydrolase apyrase or a purinergic receptor antagonist suramin. Taken together, mechanical stretch induces Ca2+ influx independently of conventional stretch-sensitive ion channels, the actin cytoskeleton, and released ATP. (C) 2014 Elsevier Inc. All rights reserved.
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