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首页> 外文期刊>Journal of Cellular Physiology >Involvement of CaMK-IIδ and gelsolin in Cd2+-dependent cytoskeletal effects in mesangial cells
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Involvement of CaMK-IIδ and gelsolin in Cd2+-dependent cytoskeletal effects in mesangial cells

机译：参与CaMK-IIδgelsolinCd2 +端依赖在系膜细胞骨架的影响细胞

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摘要

Cadmium is a toxic metal with pleiotropic effects on cell death and survival. The mesangial cell is particularly responsive to Cd's effects on kinase signaling pathways and cytoskeletal dynamics. Here we show that CaMK-II is a participant in the cytoskeletal effects of Cd2+. A major mesangial cell isoform, CaMK-IIδ, was identified in pellets of DNase I pull-downs and cytosolic immunoprecipitates of G-actin. CaMK-IIδ was also present in Triton X-100-insoluble cytoskeletal preparations and translocated to the cytoskeleton in a concentration-dependent manner in Cd-treated cells. Translocation was suppressed by KN93, an inhibitor of CaMK-II phosphorylation. In vitro actin polymerization studies indicated that recombinant CaMK-IIδ sequestered actin monomer. Cytoskeletal preparations from Cd-treated cells decrease the rate of polymerization, but KN93 co-treatment prevents this effect. Over-expressed CaMK-IIδ also translocated to the cytoskeleton upon Cd exposure, and this was prevented by KN93. Conversely, siRNA silencing of CaMK-IIδ increases the effect of cytoskeletal extracts on actin polymerization, and abrogates the effect of Cd. The actin capping and severing protein, gelsolin, translocates to the cytoskeleton in the presence of Cd2+, dependent upon the phosphorylation of CaMK-II, and is recovered together with actin and CaMK-IIδ in G-actin pull-downs and F-actin sedimentation. Translocation is accompanied by generation of a 50kDa gelsolin fragment whose appearance is prevented by KN93 and CaMK-IIδ silencing. We conclude that cytoskeletal effects of Cd in mesangial cells are partially mediated by Cd-dependent activation of CaMK-IIδ, binding of CaMK-IIδ and gelsolin to actin filaments, and cleavage of gelsolin.
机译：镉是一种有毒金属和多效性的影响细胞死亡和生存。特别是对Cd对激酶的影响信号通路和细胞骨架动力学。在这里,我们表明,CaMK-II的参与者Cd2 +细胞骨架的影响。细胞同种型,CaMK-IIδ,被发现在球团矿DNase我在下拉菜单和胞质G-actin免疫沉淀反应。在特里同x - 100不溶性细胞骨架准备并转移到细胞骨架在Cd-treated浓度的方式细胞。CaMK-II磷酸化抑制剂。表明肌动蛋白聚合研究重组CaMK-IIδ隔离肌动蛋白单体。从Cd-treated细胞细胞骨架的准备工作降低聚合的速率,但KN93co-treatment防止这种效果。CaMK-IIδ也转移到细胞骨架在Cd曝光,这被KN93阻止。相反,siRNA沉默CaMK-IIδ增加在肌动蛋白细胞骨架提取的影响聚合,废除Cd的效果。肌动蛋白限制和切断蛋白质,gelsolin,把细胞骨架的存在Cd2 +依赖的磷酸化CaMK-II,肌动蛋白和恢复CaMK-IIδ在G-actin在下拉菜单和f -肌动蛋白沉积。代的50 kda gelsolin片段的外表由KN93阻止,CaMK-IIδ沉默。系膜细胞介导的Cd由Cd-dependent激活CaMK-IIδ,绑定肌动蛋白丝的CaMK-IIδ和gelsolin,gelsolin的乳沟。

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