| Literature DB >> 26108355 |
Shulan Qiu1,2,3, Zhicheng Xiao1,2,3, Chunmei Piao1,2,3, Jing Zhang1,2,3, Yanjun Dong1,2,3, Wei Cui1,2,3, Xin Liu4, Youyi Zhang5, Jie Du1,2,3.
Abstract
TGFβ1/Smad, Wnt/β-catenin and snail1 are preferentially activated in renal tubular epithelia after injury, leading to epithelial-mesenchymal transition (EMT). The stress response is coupled to EMT and kidney injury; however, the underlying mechanism of the stress response in EMT remains elusive. AMP-activated protein kinase (AMPK) signalling is responsive to stress and regulates cell energy balance and differentiation. We found that knockdown of AMPKα, especially AMPKα2, enhanced EMT by up-regulating β-catenin and Smad3 in vitro. AMPKα2 deficiency enhanced EMT and fibrosis in a murine unilateral ureteral obstruction (UUO) model. AMPKα2 deficiency also increased the expression of chemokines KC and MCP-1, along with enhanced infiltration of inflammatory cells into the kidney after UUO. CK2β interacted physically with AMPKα and enhanced AMPKα Thr172 phosphorylation and its catalytic activity. Thus, activated AMPKα signalling suppresses EMT and secretion of chemokines in renal tubular epithelia through interaction with CK2β to attenuate renal injury.Entities:
Keywords: AMPKα2; CK2β; EMT; fibrosis; renal inflammation
Mesh：
Substances：
Year: 2015 PMID： 26108355 DOI： 10.1002/path.4579
Source DB: PubMed Journal: J Pathol ISSN： 0022-3417 Impact factor: 7.996