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首页> 外文期刊>American Journal of Physiology >Effects of chronic portal hypertension on small heat-shock proteins in mesenteric arteries.
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Effects of chronic portal hypertension on small heat-shock proteins in mesenteric arteries.

机译：慢性门脉高压对肠系膜动脉小热激蛋白的影响。

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摘要

Previous studies have shown that impaired vasoconstrictor function in chronic portal hypertension is mediated via cAMP-dependent events. Recent data have implicated two small heat-shock proteins (HSP), namely HSP20 and HSP27, in the regulation of vascular tone. Phosphorylation of HSP20 is associated with vasorelaxation, whereas phosphorylation of HSP27 is associated with vasoconstriction. We hypothesized that alterations in the expression and/or phosphorylation of small HSPs may play a role in impaired vasoconstriction in portal hypertension. A rat model of prehepatic chronic portal hypertension was used. Studies were conducted in small mesenteric arteries isolated from normal and portal hypertensive rats. Protein levels of HSP20 and HSP27 were detected by Western blot analysis. Protein phosphorylation was analyzed by isoelectric focusing. HSP20 mRNA expression was determined by RT-PCR. To examine the role of cAMP in the regulation of small HSP phosphorylation and expression, we treated both normal andportal hypertensive vessels with a PKA inhibitor Rp-cAMPS. We found both an increased HSP20 phosphorylation and a decreased HPS20 protein level in portal hypertension, both of which were restored to normal by PKA inhibition. However, PKA did not change HSP20 mRNA expression. We conclude that decreased HSP20 protein level is mediated by cAMP-dependent pathway and that impaired vasoconstrictor function in portal hypertension may be partially explained by decreased expression of HSP20. We also suggest that the phosphorylation of HSP20 by PKA may alter HSP20 turnover.
机译：先前的研究表明，慢性门脉高压症中血管收缩功能受损是通过cAMP依赖性事件介导的。最近的数据已暗示了两种小的热休克蛋白（HSP），即HSP20和HSP27，可以调节血管紧张度。 HSP20的磷酸化与血管舒张相关，而HSP27的磷酸化与血管收缩相关。我们假设小HSP的表达和/或磷酸化的改变可能在门脉高压的血管收缩受损中起作用。使用大鼠肝前慢性门脉高压模型。在从正常和门脉高压大鼠中分离出的小肠系膜动脉中进行了研究。通过蛋白质印迹分析检测HSP20和HSP27的蛋白水平。通过等电聚焦分析蛋白质的磷酸化。通过RT-PCR确定HSP20 mRNA表达。为了检查cAMP在调节小HSP磷酸化和表达中的作用，我们用PKA抑制剂Rp-cAMPS处理了正常和门脉高压血管。我们发现门脉高压症中HSP20磷酸化水平升高和HPS20蛋白水平降低，两者均通过PKA抑制而恢复正常。但是，PKA并没有改变HSP20 mRNA的表达。我们得出的结论是，HSP20蛋白水平的降低是由cAMP依赖性途径介导的，门脉高压中血管收缩功能的受损可能部分由HSP20的表达降低所解释。我们还建议，PKA将HSP20磷酸化可能会改变HSP20的周转率。

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