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学科主题: 基础医学
题名:
AMPK2 reduces renal epithelial transdifferentiation and inflammation after injury through interaction with CK2
作者: 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
发表日期: 2015-11-01
DOI: 10.1002/path.4579
卷: 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
所属项目编号: 31090363 ; 81000871 ; 81301797 ; 2009CB522205 ; 2012CB945104 ; PXM 2013_014226_07_000088
项目资助者: National Natural Science Foundation of China ; Chinese Ministry of Science and Technology ; Beijing Collaborative Research Centre for Cardiovascular Disease
WOS记录号: WOS:000363211000007
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57710
Appears in Collections:基础医学院_期刊论文

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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

Recommended Citation:
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.
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