焦磷酸核苷酸和缓激肽刺激乳腺肿瘤细胞中通过钙离子增加介导的花生四烯酸释放。

Release of arachidonic acid via Ca2+ increase stimulated by pyrophosphonucleotides and bradykinin in mammary tumour cells.

作者信息

Enomoto K, Furuya K, Yamagishi S, Oka T, Maeno T

机构信息

Department of Physiology, Shimane Medical University, Japan.

出版信息

Cell Biochem Funct. 1995 Dec;13(4):279-86. doi: 10.1002/cbf.290130409.

DOI:10.1002/cbf.290130409

PMID:8565149

Abstract

The relationship between the increase of intracellular Ca2+ and the release of arachidonic acid by bradykinin and pyrophosphonucleotides was studied in cultured mammary tumour cells, MMT060562. Bradykinin, ATP, UTP and UDP induced an increase of intracellular Ca2+ and the release of arachidonic acid from phospholipids into the extracellular fluid. Release of arachidonic acid was also induced by the application of the Ca2+ ionophore, A23187. Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist. It is suggested that the increase in cytosolic Ca(2+)-induced release of arachidonic acid occurs through activation of calmodulin-dependent phospholipase A2.

摘要

在培养的乳腺肿瘤细胞MMT060562中，研究了细胞内Ca2+增加与缓激肽和焦磷酸核苷酸释放花生四烯酸之间的关系。缓激肽、ATP、UTP和UDP可诱导细胞内Ca2+增加，并使花生四烯酸从磷脂释放到细胞外液中。应用Ca2+离子载体A23187也可诱导花生四烯酸的释放。磷脂酶A2的阻滞剂米帕林和钙调蛋白拮抗剂W-7可减少缓激肽和ATP引起的花生四烯酸释放。提示胞质Ca(2+)增加诱导的花生四烯酸释放是通过钙调蛋白依赖性磷脂酶A2的激活实现的。