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首页> 外文期刊>Journal of Cellular Physiology >Possible involvement of heat shock protein 25 in the angiotensin II-induced glomerular mesangial cell contraction via p38 MAP kinase.
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Possible involvement of heat shock protein 25 in the angiotensin II-induced glomerular mesangial cell contraction via p38 MAP kinase.

机译：热休克蛋白25日在参与的可能性血管紧张素II-induced肾小球系膜通过地图p38激酶细胞收缩。

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摘要

In the rat kidney, mesangial cells (MCs), especially those in the extraglomerular mesangium (EGM) region of the juxtagomerular apparatus, express high amounts of heat shock protein 25 (HSP25). Because MCs are contractile in vivo and HSP25 is known to modulate polymerization/depolymerization of F-actin and to be involved in smooth muscle contraction, it is possible that HSP25 participates in the contraction process of MCs. We analyzed a permanent mouse MC line using Northern and Western blot analyses, and observed that similar to the MCs in the glomerulus, these cells also express high amounts of HSP25 constitutively. Exposure of these cells to angiotensin II (ANG II: 2 x 10(-7) M) evoked contraction and a concomitant increase in HSP25 phosphorylation, while the cytoplasmic fraction of HSP25 was transiently reduced. Because phosphorylation of HSP25 is essential for its actin-modulating function, we suppressed the activity of p38 MAP kinase, the major upstream activator of HSP25 phosphorylation, with the specific inhibitor SB 203580. This maneuver reduced HSP25 phosphorylation dramatically, abolished cell contraction, and prevented the decrease of the cytoplasmic HSP25 content. This suggests that HSP25 might be a component of the contraction machinery in MCs and that this process depends on p38 MAP kinase-mediated HSP25 phosphorylation. The decrease of cytoplasmic HSP25 content observed after ANG II exposure is probably the result of a transient redistribution of HSP25 into a buffer-insoluble fraction, because the whole cell content of HSP25 did not change, a phenomenon known to be related to the actin-modulating activity of HSP25. The fact that this function requires phosphorylation of HSP25 would explain the observation that HSP25 does not redistribute in SB 203580-pretreated cells. Copyright 1999 Wiley-Liss, Inc.
机译：大鼠肾脏系膜细胞(mc),尤其是extraglomerular肾小球膜(临时)地区juxtagomerular仪器,表达大量的热休克蛋白25(HSP25)。HSP25调节f -肌动蛋白聚合/解聚,参与平滑肌收缩,它是可能HSP25参与收缩MCs的过程。永久的鼠标使用北部和MC线免疫印迹分析,观察到相似的肾小球的MCs,这些细胞也表达大量的HSP25既定的。接触这些细胞的血管紧张素ⅱ(ANG2: 2 x 10(7)米)诱发和收缩伴随增加HSP25磷酸化,虽然HSP25的细胞质分数暂时性的减少。HSP25 actin-modulating是至关重要的函数,我们压制人们的活动地图HSP25主要上游激酶活化剂磷酸化,特定抑制剂某人203580. 磷酸化作用显著,废除了细胞收缩,预防减少的细胞质HSP25内容。HSP25收缩的可能是一个组成部分这个过程取决于机械在MCs和p38地图kinase-mediated HSP25磷酸化。的减少细胞质HSP25内容ANGⅱ暴露可能是后观察HSP25瞬态重新分配的结果成buffer-insoluble分数,因为整个单元的内容HSP25并未改变,现象有关actin-modulating HSP25的活动。这个函数需要HSP25的磷酸化可以解释观察HSP25不在某人203580 -预处理细胞重新分配。版权1999 Wiley-Liss公司。

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