Kruger H, Carr S, Brennand J C, McLean J S
Department of Biological Sciences, University of Paisley, Scotland.
Biochem Biophys Res Commun. 1995 Dec 5;217(1):52-8. doi: 10.1006/bbrc.1995.2744.
The signalling pathways used by the human endothelin A receptor to activate phospholipase A2 in Chinese hamster ovary cells were investigated. Pertussis toxin caused a partial but significant reduction in endothelin-1-induced arachidonic acid release although cAMP-dependent kinase inhibitors did not mimic its action. Extracellular calcium and its entry into the cell was essential for activation of phospholipase A2 as its removal from media or incubation with an intracellular calcium chelator-reduced activation. Nifedipine had no effect on endothelin-1-induced arachidonic acid release while divalent cations caused a significant reduction indicating the possible role of CRAC. Thapsigargin caused an increase in arachidonic acid release which was completely inhibited by pertussis toxin treatment. This further supports the involvement of CRAC in calcium influx and activation of phospholipase A2 by the human endothelin A receptor.
研究了人内皮素A受体在中国仓鼠卵巢细胞中激活磷脂酶A2所使用的信号通路。百日咳毒素导致内皮素-1诱导的花生四烯酸释放部分但显著减少，尽管cAMP依赖性激酶抑制剂不能模拟其作用。细胞外钙及其进入细胞对于磷脂酶A2的激活至关重要，因为从培养基中去除钙或与细胞内钙螯合剂孵育会降低激活。硝苯地平对内皮素-1诱导的花生四烯酸释放没有影响，而二价阳离子则导致显著减少，表明CRAC可能发挥作用。毒胡萝卜素导致花生四烯酸释放增加，而百日咳毒素处理可完全抑制这种增加。这进一步支持了CRAC参与人内皮素A受体介导的钙内流和磷脂酶A2激活的观点。
