IR@PKUHSC  > 北京大学基础医学院
学科主题基础医学
AMPK2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2
Qiu, Shulan1,2,3; Xiao, Zhicheng1,2,3; Piao, Chunmei1,2,3; Zhang, Jing1,2,3; Dong, Yanjun1,2,3; Cui, Wei1,2,3; Liu, Xin4; Zhang, Youyi5; Du, Jie1,2,3
关键词Ampk2 Ck2 Emt Renal Inflammation Fibrosis
刊名JOURNAL OF PATHOLOGY
2015-11-01
DOI10.1002/path.4579
237期:3页:330-342
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Pathology
研究领域[WOS]Oncology ; Pathology
关键词[WOS]ACTIVATED PROTEIN-KINASE ; FIREFLY LUCIFERASE COMPLEMENTATION ; ENDOPLASMIC-RETICULUM STRESS ; MESENCHYMAL TRANSITION ; CHEMOKINE PRODUCTION ; KIDNEY-DISEASE ; CELLS ; EXPRESSION ; FIBROSIS ; SUBUNIT
英文摘要

TGF1/Smad, Wnt/-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 AMPK, especially AMPK2, enhanced EMT by up-regulating -catenin and Smad3 in vitro. AMPK2 deficiency enhanced EMT and fibrosis in a murine unilateral ureteral obstruction (UUO) model. AMPK2 deficiency also increased the expression of chemokines KC and MCP-1, along with enhanced infiltration of inflammatory cells into the kidney after UUO. CK2 interacted physically with AMPK and enhanced AMPK Thr172 phosphorylation and its catalytic activity. Thus, activated AMPK signalling suppresses EMT and secretion of chemokines in renal tubular epithelia through interaction with CK2 to attenuate renal injury. Copyright (c) 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

语种英语
WOS记录号WOS:000363211000007
项目编号31090363 ; 81000871 ; 81301797 ; 2009CB522205 ; 2012CB945104 ; PXM 2013_014226_07_000088
资助机构National Natural Science Foundation of China ; Chinese Ministry of Science and Technology ; Beijing Collaborative Research Centre for Cardiovascular Disease
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57710
专题北京大学基础医学院
作者单位1.Capital Med Univ, Beijing Anzhen Hosp, Beijing 100029, Peoples R China
2.Minist Educ, Key Lab Remodeling Related Cardiovasc Dis, Beijing, Peoples R China
3.Beijing Inst Heart Lung & Blood Vessel Dis, Beijing, Peoples R China
4.Chinese Acad Sci, Ctr Mol Syst Biol, Inst Genet & Dev Biol, Beijing, Peoples R China
5.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Lab Cardiovasc Bioact Mol, Beijing 100871, Peoples R China
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GB/T 7714
Qiu, Shulan,Xiao, Zhicheng,Piao, Chunmei,et al. AMPK2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2[J]. JOURNAL OF PATHOLOGY,2015,237(3):330-342.
APA Qiu, Shulan.,Xiao, Zhicheng.,Piao, Chunmei.,Zhang, Jing.,Dong, Yanjun.,...&Du, Jie.(2015).AMPK2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2.JOURNAL OF PATHOLOGY,237(3),330-342.
MLA Qiu, Shulan,et al."AMPK2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2".JOURNAL OF PATHOLOGY 237.3(2015):330-342.
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