RECEPTOR-MEDIATED METABOLISM OF THE PHOSPHOINOSITIDES AND PHOSPHATIDIC-ACID IN RAT LACRIMAL ACINAR-CELLS
RECEPTOR-MEDIATED METABOLISM OF THE PHOSPHOINOSITIDES AND PHOSPHATIDIC-ACID IN RAT LACRIMAL ACINAR-CELLS
复制标题
DOI：
10.1042/bj2180187
复制
发表时间：
1984-01-01
影响因子：
4.1
通讯作者：
PUTNEY, JW
中科院分区：
文献类型：
--
作者：
GODFREY, PP;PUTNEY, JW
The metabolism of the inositol lipids and phosphatidic acid in rat lacrimal acinar cells was investigated. The muscarinic cholinergic agonist methacholine caused a rapid loss of 15% of [32P]phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] and a rapid increase in [32P]phosphatidic acid (PtdA). Chemical measurements indicated that the changes in 32P labeling of these lipids closely resembled changes in their total cellular content. Chelation of extracellular Ca2+ with excess EGTA [ethylene glycal bis(.beta.-aminoethyl ether)N,N''-tetraacetic acid] caused a significant decrease in the PtdA labeling and an apparent loss of PtdIns(4,5)P2 breakdown. The Ca ionophores A23187 [calcimycin] and ionomycin provoked a substantial breakdown of [32P]PtdIns(4,5)P2 and phosphatidylinosital 4-phosphate (PtdIns4P); a decrease in [32P]PtdA was also observed. Increased in inositol phosphate, inositol bisphosphate and inositol trisphosphate were observed in methacholine-stimulated cells, and this increase was greatly amplified in the presence of 10 mM-LiCl; .alpha.-adrenergic stimulation also caused a substantial increase in inositol phosphates. A23187 provoked a much smaller increase in the formation of inositol phosphates than did either methacholine or adrenaline [epinephrine]. Experiments with excess extracellular EGTA and with a protocol that eliminates intracellular Ca2+ release indicated that the labeling of inositol phosphates was partially dependent on the presence of extracellular Ca2+ and independent of intracellular Ca2+ mobilization. In the rat lacrimal gland, there appears to be a rapid phospholipase C-mediated breakdown of PtdIns(4,5)P2 and a synthesis of PtdA, in response to activation of receptors that bring about an increase in intracellular Ca2+. The results are consistent with a role for these lipids early in the stimulus-response pathway of the lacrimal acinar cell.
