中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Adiponectin deficiency impairs liver regeneration through attenuating stat3 phosphorylation in mice

文献类型:期刊论文

作者Shu, Run-Zhe4; Zhang, Feng4; Wang, Fang2; Feng, De-Chun4; Li, Xi-Hua2; Ren, Wei-Hua2,3; Wu, Xiao-Lin2; Yang, Xue2; Liao, Xiao-Dong2; Huang, Lei2
刊名Laboratory investigation
出版日期2009-09-01
卷号89期号:9页码:1043-1052
关键词Cell proliferation Hepatic steatosis Knockout mice Partial hepatectomy Socs3 Stat3 Ppar alpha
ISSN号0023-6837
DOI10.1038/labinvest.2009.63
通讯作者Wang, zhu-gang(zhugangw@shsmu.edu.cn)
英文摘要Liver regeneration is a very complex and well-orchestrated process associated with signaling cascades involving cytokines, growth factors, and metabolic pathways. adiponectin is an adipocytokine secreted by mature adipocytes, and its receptors are widely distributed in many tissues, including the liver. adiponectin has direct actions in the liver with prominent roles to improve hepatic insulin sensitivity, increase fatty acid oxidation, and decrease inflammation. to test the hypothesis that adiponectin is required for normal progress of liver regeneration, 2/3 partial hepatectomy (ph) was performed on wild-type and adiponectin-null mice. compared to wild-type mice, adiponectin-null mice displayed decreased liver mass regrowth, impeded hepatocyte proliferation, and increased hepatic lipid accumulation. gene expression analysis revealed that adiponectin regulated the gene transcription related to lipid metabolism. furthermore, the suppressed hepatocyte proliferation was accompanied with reduced signal transducer and activator of transcription protein 3 (stat3) activity and enhanced suppressor of cytokine signaling 3 (socs3) transcription. in conclusion, adiponectin-null mice exhibit impaired liver regeneration and increased hepatic steatosis. increased expression of socs3 and subsequently reduced activation of stat3 in adiponectin-null mice may contribute to the alteration of the liver regeneration capability and hepatic lipid metabolism after ph. laboratory investigation (2009) 89, 1043-1052; doi:10.1038/labinvest.2009.63; published online 29 june 2009
WOS关键词PARTIAL-HEPATECTOMY ; PRIMARY NONFUNCTION ; HEPATIC STEATOSIS ; KNOCKOUT MICE ; OBESE MICE ; MOUSE ; ALPHA ; ACID ; EXPRESSION ; PROTEIN
WOS研究方向Research & Experimental Medicine ; Pathology
WOS类目Medicine, Research & Experimental ; Pathology
语种英语
WOS记录号WOS:000269323600008
出版者NATURE PUBLISHING GROUP
URI标识http://www.irgrid.ac.cn/handle/1471x/2400753
专题中国科学院大学
通讯作者Wang, Zhu-Gang
作者单位1.Shanghai Jiao Tong Univ, Sch Med, Dept Med Genet,Key Lab Stem Cell Biol,Inst Hlth S, Chinese Acad Sci,Shanghai Inst Biol Sci, Shanghai 200025, Peoples R China
2.Shanghai Jiao Tong Univ, Sch Med, Dept Med Genet, Shanghai Univ,E Inst, Shanghai 200025, Peoples R China
3.Shanghai Res Ctr Model Organisms, Shanghai, Peoples R China
4.Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China
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GB/T 7714
Shu, Run-Zhe,Zhang, Feng,Wang, Fang,et al. Adiponectin deficiency impairs liver regeneration through attenuating stat3 phosphorylation in mice[J]. Laboratory investigation,2009,89(9):1043-1052.
APA Shu, Run-Zhe.,Zhang, Feng.,Wang, Fang.,Feng, De-Chun.,Li, Xi-Hua.,...&Wang, Zhu-Gang.(2009).Adiponectin deficiency impairs liver regeneration through attenuating stat3 phosphorylation in mice.Laboratory investigation,89(9),1043-1052.
MLA Shu, Run-Zhe,et al."Adiponectin deficiency impairs liver regeneration through attenuating stat3 phosphorylation in mice".Laboratory investigation 89.9(2009):1043-1052.

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来源:中国科学院大学

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