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首页> 外文期刊>American Journal of Physiology >Calmodulin and protein kinase C regulate gap junctional coupling in lens epithelial cells.
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Calmodulin and protein kinase C regulate gap junctional coupling in lens epithelial cells.

机译：钙调蛋白和蛋白激酶C调节晶状体上皮细胞中的间隙连接偶联。

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摘要

The mechanisms regulating the permeability of lens epithelial cell gap junctions in response to calcium ionophore or ATP agonist-mediated increases in cytosolic Ca2+ (Cai2+) have been investigated using inhibitors of calmodulin (CaM) and PKC. Cell-to-cell transfer of the fluorescent dye AlexaFluor594 decreased after the rapid and sustained increase in Cai2+ (to micromolar concentrations) observed after the addition of ionophore plus Ca2+ but was prevented by pretreatment with inhibitors of CaM but not PKC. In contrast, the delayed, transient decrease in cell-to-cell coupling observed after the addition of ATP that we have reported previously (Churchill G, Lurtz MM, and Louis CF. Am J Physiol Cell Physiol 281: C972-C981, 2001) could be prevented by either the direct or indirect inhibition of PKC but not by inhibition of CaM. Surprisingly, there was no change in the relative proportion of the different phosphorylated forms of lens connexin43 after this ATP-dependent transient decrease in cell-to-cell coupling. Although BAPTA-loaded cells did not display the ATP-dependent transient increase in Cai2+, the delayed, transient decrease in cell-to-cell dye transfer was still observed, indicating it was Cai2+ independent. Thus CaM-mediated inhibition of lens gap junctions is associated with sustained, micromolar Cai2+ concentrations, whereas PKC-mediated inhibition of lens gap junctions is associated with agonist activation of second messenger pathways that are independent of changes in Cai2+.
机译：已使用钙调蛋白（CaM）和PKC抑制剂研究了调节钙离子载体或ATP激动剂介导的胞质Ca2 +（Cai2 +）调节晶状体上皮细胞间隙连接的通透性的机制。加入离子载体加Ca2 +后，Ca2 +迅速且持续增加（至微摩尔浓度），荧光染料AlexaFluor594的细胞间转移减少，但通过用CaM抑制剂而非PKC进行预处理阻止了这种行为。相反，我们先前报道的添加ATP后观察到的细胞间偶联延迟的瞬时降低（Churchill G，Lurtz MM和Louis CF. Am J Physiol Cell Physiol 281：C972-C981，2001）可以通过直接或间接抑制PKC来预防，但不能通过抑制CaM来预防。出人意料的是，在细胞与细胞之间的这种ATP依赖性瞬时减少之后，晶状体连接蛋白43的不同磷酸化形式的相对比例没有变化。尽管加载BAPTA的细胞在Cai2 +中没有显示ATP依赖性的瞬时增加，但仍观察到细胞间染料转移的延迟，瞬时减少，表明它是与Cai2 +无关的。因此，CaM介导的晶状体间隙连接的抑制与持续的微摩尔Cai2 +浓度相关，而PKC介导的晶状体间隙连接的抑制与第二信使途径的激动剂活化相关，所述第二信使途径与Cai2 +的变化无关。

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