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C16-神经酰胺诱导的F-肌动蛋白调节刺激小鼠胚胎干细胞迁移:N-WASP/Cdc42/Arp2/3复合物和丝切蛋白-1/α-辅肌动蛋白的参与

C(16)-Ceramide-induced F-actin regulation stimulates mouse embryonic stem cell migration: involvement of N-WASP/Cdc42/Arp2/3 complex and cofilin-1/α-actinin.

作者信息

Park Su Shin, Kim Mi Ok, Yun Seung Pil, Ryu Jung Min, Park Jae Hong, Seo Bit Na, Jeon Ji Hoon, Han Ho Jae

机构信息

Department of Veterinary Physiology, Biotherapy Human Resources Center (BK 21), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.

出版信息

Biochim Biophys Acta. 2013 Feb;1831(2):350-60. doi: 10.1016/j.bbalip.2012.09.005. Epub 2012 Sep 15.

Abstract

Ceramide, a major structural element in the cellular membrane, is a key regulatory factor in various cellular behaviors that are dependent on ceramide-induced association of specific proteins. However, molecular mechanisms that regulate ceramide-induced embryonic stem cell (ESC) migration are still not well understood. Thus, we investigated the effect of ceramide on migration and its related signal pathways in mouse ESCs. Among ceramide species with different fatty acid chain lengths, C(16)-Cer increased migration of mouse ESCs in a dose- (≥1μM) and time-dependent (≥8h) manners, as determined by the cell migration assay. C(16)-Cer (10μM) increased protein-kinase C (PKC) phosphorylation. Subsequently, C(16)-Cer increased focal adhesion kinase (FAK) and Paxillin phosphorylation, which were inhibited by PKC inhibitor Bisindolylmaleimide I (1μM). When we examined for the downstream signaling molecules, C(16)-Cer activated small G protein (Cdc42) and increased the formation of complex with Neural Wiskott-Aldrich Syndrome Protein (N-WASP)/Cdc42/Actin-Related Protein 2/3 (Arp2/3). This complex formation was disrupted by FAK- and Paxillin-specific siRNAs. Furthermore, C(16)-Cer-induced increase of filamentous actin (F-actin) expression was inhibited by Cdc42-, N-WASP-, and Arp2/3-specific siRNAs, respectively. Indeed, C(16)-Cer increased cofilin-1/F-actin interaction or F-actin/α-actinin-1 and α-actinin-4 interactions in the cytoskeleton compartment, which was reversed by Cdc42-specific siRNA. Finally, C(16)-Cer-induced increase of cell migration was inhibited by knocking down each signal pathway-related molecules with siRNA or inhibitors. In conclusion, C(16)-Cer enhances mouse ESC migration through the regulation of PKC and FAK/Paxillin-dependent N-WASP/Cdc42/Arp2/3 complex formation as well as through promoting the interaction between cofilin-1 or α-actinin-1/-4 and F-actin.

摘要

神经酰胺是细胞膜中的一种主要结构成分,是各种细胞行为中的关键调节因子,这些细胞行为依赖于神经酰胺诱导的特定蛋白质的结合。然而,调节神经酰胺诱导的胚胎干细胞(ESC)迁移的分子机制仍未完全清楚。因此,我们研究了神经酰胺对小鼠胚胎干细胞迁移及其相关信号通路的影响。在具有不同脂肪酸链长度的神经酰胺种类中,通过细胞迁移试验确定,C(16)-神经酰胺以剂量(≥1μM)和时间依赖性(≥8小时)的方式增加小鼠胚胎干细胞的迁移。C(16)-神经酰胺(10μM)增加蛋白激酶C(PKC)的磷酸化。随后,C(16)-神经酰胺增加粘着斑激酶(FAK)和桩蛋白的磷酸化,这被PKC抑制剂双吲哚马来酰亚胺I(1μM)抑制。当我们检测下游信号分子时,C(16)-神经酰胺激活小G蛋白(Cdc42),并增加与神经威斯科特-奥尔德里奇综合征蛋白(N-WASP)/Cdc42/肌动蛋白相关蛋白2/3(Arp2/3)的复合物形成。这种复合物的形成被FAK和桩蛋白特异性小干扰RNA(siRNA)破坏。此外,C(16)-神经酰胺诱导的丝状肌动蛋白(F-肌动蛋白)表达增加分别被Cdc42、N-WASP和Arp2/3特异性siRNA抑制。事实上,C(16)-神经酰胺增加了细胞骨架区室中丝切蛋白-1/F-肌动蛋白相互作用或F-肌动蛋白/α-辅肌动蛋白-1和α-辅肌动蛋白-4相互作用,这被Cdc42特异性siRNA逆转。最后,通过用siRNA或抑制剂敲低每个信号通路相关分子,抑制了C(16)-神经酰胺诱导的细胞迁移增加。总之,C(16)-神经酰胺通过调节PKC和FAK/桩蛋白依赖性N-WASP/Cdc42/Arp2/3复合物的形成以及促进丝切蛋白-1或α-辅肌动蛋白-1/-4与F-肌动蛋白之间的相互作用来增强小鼠胚胎干细胞的迁移。

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