Cofilin participates in regulating alpha-epithelial sodium channel by interaction with 14-3-3 isoforms
Ashfaq-Ahmad-Shah Bukhari1
Xue Zhang1
Min Li2
Anran Zhao1
Hao Dong1
Xiubin Liang3
1.Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166,China2.Department of Pathology, Nanjing Medical University, Nanjing, Jiangsu 211166,China3.Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166,China;Department of Nephrology, the Affiliated Sir Run Run Hospital of Nanjing Medical University, Nanjing, Jiangsu 211166, China
摘要：Renal epithelial sodium channel (ENaC) plays a crucial role in maintaining homeostasis and sodium absorption.While insulin participates in controlling sodium transport across the renal epithelium,the underlying molecular mechanism remain unclear.In this study,we found that insulin increased the expression and function of alphaepithelial sodium channel (α-ENaC) as well as phosphorylation of cofilin,a family of actin-binding proteins which disassembles actin filaments,in mouse cortical collecting duct (mpkCCDc14) cells.The wild-type (WT) cofilin and its constitutively phosphorylated form (S3D),but not its constitutively non-phosphorylable form (S3A),contributed to the elevated expression on α-ENaC.Overexpression of 14-3-3ε,β,or γ increased the expression of α-ENaC and cofilin phosphorylation,which was blunted by knockdown of 14-3-3ε,β,or γ.Moreover,it was found that insulin increased the interaction between cofilin and 14-3-3 isoforms,which indicated relevance of 14-3-3 isoforms with cofilin.Furthermore,LIMK1/SSH1 pathway was involved in regulation of cofilin and α-ENaC expression by insulin.The results from this work indicate that cofilin participates in the regulation of α-ENaC by interaction with 14-3-3 isoforms.
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分类号：R692.6(泌尿科学（泌尿生殖系疾病）)
论文发表日期：2020-09-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 351-360 )
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