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首页> 外文期刊>Journal of Cellular Physiology >Involvement of tyrosine kinase in the hypoxia/reoxygenation-induced gap junctional intercellular communication abnormality in cultured human umbilical vein endothelial cells.
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Involvement of tyrosine kinase in the hypoxia/reoxygenation-induced gap junctional intercellular communication abnormality in cultured human umbilical vein endothelial cells.

机译：酪氨酸激酶参与缺氧/ reoxygenation-induced交界的差距细胞间通讯异常人类脐静脉内皮细胞培养。

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摘要

Vascular endothelial cells (EC), communicating with one another across gap junctions, are usually made dysfunctional by hypoxia and reoxygenation (H/R); however, very limited information exists regarding the effects of H/R on the endothelial gap junctions. We investigated whether H/R interferes with endothelial gap junctional intercellular communication (GJIC). After human umbilical vein EC had grown to confluence, they were exposed to hypoxia (pO2 < 0.1%) for 12-16 h and then returned to normal atmospheric conditions for reoxygenation. At 0-, 2-, 4-, 6-h reoxygenation, GJIC was detected by means of a fluorescence recovery after a photobleaching technique. The results demonstrated that a GJIC reduction (about 20% less than that under normoxia) was induced after 2 h of reoxygenation; after 4 h of reoxygenation, it began to recover (to about 10% less than that under normoxia); and after 6 h of reoxygenation, GJIC was restored to the normal level. Calphostin C (1 x 10(-7) mol/l), a specific protein kinase C inhibitor, partially inhibited the reduction in GJIC (resulting in a level about 10% less than that under normoxia), whereas the tyrosine kinase inhibitor genistein (10 micromol/L) completely blocked the reduction in GJIC. Vanadate (1.5 mmol/l), a tyrosine phosphatase inhibitor, amplified the inhibitory effect of H/R on GJIC (to about 40% less than that under normoxia). Immunofluorescence and immunoprecipitation showed that 2-h reoxygenation significantly stimulated tyrosine protein phosphorylation, and this phosphorylation event was obviously enhanced by vanadate. The results of Western blotting showed that the gap junctional protein connexin 43 (Cx43) was phosphorylated by H/R; moreover, immunoprecipitation demonstrated that 2-h reoxygenation induced a prominent increase of tyrosine phosphorylation of Cx43 compared with that under normoxia. These data indicate that H/R induces a transient endothelial GJIC dysfunction through the activation of tyrosine kinase and phosphorylation of tyrosine residues of Cx43.
机译：血管内皮细胞(EC),交流在缝隙连接彼此,通常由缺氧和功能失调复氧(H / R);信息存在关于H / R的影响在内皮缝隙连接。是否H / R干扰内皮差距交叉的细胞间通讯(GJIC)。人类脐静脉EC已经后融合,他们暴露于低氧(警察乙<0.1%) 12 - 16 h,然后恢复正常大气复氧条件。2 - 4 - 6小时再氧化,GJIC被检测到后荧光恢复的手段光漂白技术。证明GJIC减少(大约20%不到,在normoxia)后被诱导2 h再氧化;它开始恢复(小于10%在normoxia);GJIC恢复到正常水平。C (1 x 10 (7) mol / l),一个特定的蛋白激酶C抑制剂,抑制了部分减少GJIC(导致水平不到10%,在normoxia),而酪氨酸激酶完全抑制染料木黄酮(10 micromol / L)封锁了GJIC的减少。更易/ l),酪氨酸磷酸酶抑制剂,放大H / R对GJIC的抑制作用(在normoxia不到40%)。免疫荧光和免疫沉淀反应, 2 h再氧化明显刺激酪氨酸蛋白磷酸化,这磷酸化事件很明显增强钒酸盐。交界的差距蛋白质联接蛋白43通过H / R (Cx43)磷酸化;免疫沉淀反应表明,2 h复氧诱导的显著增加酪氨酸的磷酸化Cx43相比normoxia下。引发一个短暂的内皮细胞GJIC功能障碍通过激活酪氨酸激酶和Cx43的磷酸化的酪氨酸残基。

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