Cell swelling activates stress-activated protein kinases, p38 MAP kinase and JNK, in renal epithelial A6 cells.
Cell swelling activates stress-activated protein kinases, p38 MAP kinase and JNK, in renal epithelial A6 cells.
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细胞肿胀会激活肾上皮 A6 细胞中的应激激活蛋白激酶、p38 MAP 激酶和 JNK。
DOI：
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Yoshinori Marunaka
中科院分区：
文献类型：
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作者：
N. Niisato;Martin Post;W. Driessche;Yoshinori Marunaka
渗透性休克被认为是激活应激激活蛋白激酶(SAPKs)、p38MAPK和c-jun氨基末端激酶(JNKs)的因素之一。在肾上皮A6细胞中，低渗休克可瞬时激活SAPKs，5min时激活最大。A6细胞暴露于低渗溶液后，肿胀后出现调节性体积减小(RVD)。而5-硝基-2-(3-苯丙氨基)苯甲酸(NPPB，一种氯离子通道阻断剂)在低渗休克90min后仍能维持SAPKs的激活，完全阻断RVD并使细胞持续肿胀。将细胞暴露在含有制霉菌素的高K(+)等渗溶液中，可导致细胞持续肿胀，也可持续激活SAPKs。此外，氯丙嗪引起的膜变形激活了SAPKs。这些结果表明，细胞肿胀或氯丙嗪引起的膜张力变化，而不是渗透压，是激活A6细胞SAPKs的重要步骤。
Osmotic shock is well recognized as one of the factors activating stress-activated protein kinases (SAPKs), p38 MAP kinase and c-Jun N-terminal kinases (JNKs). In renal epithelial A6 cells, hypo-osmotic shock transiently activated SAPKs with maximal activation at 5 min. A6 cells showed a regulatory volume decrease (RVD) after swelling when the cells were exposed to a hypo-osmotic solution. In contrast, activation of SAPKs was maintained over 90 min after hypo-osmotic shock in the presence of 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, a Cl(-) channel blocker), which completely blocked the RVD and kept the cells continuously swelling. Exposure of the cells to a high K(+) iso-osmotic solution containing nystatin, which induces continuous cell swelling, also continuously activated SAPKs. Furthermore, membrane deformation induced by chlorpromazine activated SAPKs. These results suggest that changes in membrane tension by cell swelling or chlorpromazine, but not osmolality, are important steps for activation of SAPKs in A6 cells.
影响因子：
10.5
作者：
KAMADA, Y;JUNG, US;LEVIN, DE
通讯作者：
LEVIN, DE
低渗休克和高外部 K 处理后培养的鲨鱼直肠腺细胞细胞骨架重组的共聚焦显微镜观察。
DOI：
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发表时间：
1997
期刊：
The Journal of experimental zoology.
影响因子：
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作者：
Henson,JH;Roesener,CD;Gaetano,CJ;Mendola,RJ;ForrestJr,JN;Holy,J;Kleinzeller,A
通讯作者：
Kleinzeller,A