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- Title
Effect of lysophosphatidylglycerol on intracellular free Ca<sup>2+</sup> concentration in A10 vascular smooth muscle cells.
- Authors
Zhang, Ying; Zhang, Jing-Dian; Zhu, Ming-Qin; Cui, Li; Zhang, Ming; Xu, Yan-Jun; Dhalla, Naranjan S.
- Abstract
Although plasma levels of lysophosphatidylglycerol (LPG) are increased in hypertension, its role in the pathogenesis of vascular defects is not clear. In view of the importance of Ca2+ overload in causing vascular smooth muscle (VSM) dysfunction, the action of LPG on [Ca2+]i in cultured A10 VSM cell line was examined by using Fura 2-AM acetoxymethyl ester technique. LPG was found to induce a concentration-dependent increase in [Ca2+]i in VSM cells. This change was dependent both on the extracellular and intracellular Ca2+ sources, as it was reduced by 30% by EGTA, an extracellular Ca2+ chelator, and 70% by thapsigargin, a sarcoplasmic reticulum (SR) Ca2+-pump inhibitor. However the increase in [Ca2+]i due to LPG was not altered by caffeine or ryanodine, which affect Ca2+-release through the ryanodine receptors in the SR. On the other hand, LPG-induced change in [Ca2+]i was suppressed by 2-nitro-4-carboxyphenyl N, N-diphenylcarbamate, a phospholipase C (PLC) inhibitor, as well as by xestospongin and 2-aminoethoxydiphenyl borate, two inositol trisphosphate (IP3) receptor inhibitors in the SR. These observations support the view that LPG-induced increase in [Ca2+]i in VSM cells is mainly a result of Ca2+ release from Ca2+ pool in the SR through PLC/IP3-sensitive signal transduction mechanism. Furthermore, it is suggested that the elevated level of LPG may induce intracellular Ca2+ overload and thus play a critical role in the development of vascular abnormalities.
- Subjects
VASCULAR smooth muscle; HYPERTENSION; SARCOPLASMIC reticulum; INTRACELLULAR calcium; INOSITOL trisphosphate
- Publication
Canadian Journal of Physiology & Pharmacology, 2017, Vol 95, Issue 10, p1283
- ISSN
0008-4212
- Publication type
Article
- DOI
10.1139/cjpp-2017-0127