Document Detail


IKKi deficiency promotes pressure overload-induced cardiac hypertrophy and fibrosis.
MedLine Citation:
PMID:  23349709     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The inducible IκB kinase (IKKi/IKKε) is a recently described serine-threonine IKK-related kinase. Previous studies have reported the role of IKKi in infectious diseases and cancer. However, its role in the cardiac response to pressure overload remains elusive. In this study, we investigated the effects of IKKi deficiency on the development of pathological cardiac hypertrophy using in vitro and in vivo models. First, we developed mouse models of pressure overload cardiac hypertrophy induced by pressure overload using aortic banding (AB). Four weeks after AB, cardiac function was then assessed through echocardiographic and hemodynamic measurements. Western blotting, real-time PCR and histological analyses were used to assess the pathological and molecular mechanisms. We observed that IKKi-deficient mice showed significantly enhanced cardiac hypertrophy, cardiac dysfunction, apoptosis and fibrosis compared with WT mice. Furthermore, we recently revealed that the IKKi-deficient mice spontaneously develop cardiac hypertrophy. Moreover, in vivo experiments showed that IKKi deficiency-induced cardiac hypertrophy was associated with the activation of the AKT and NF-κB signaling pathway in response to AB. In cultured cells, IKKi overexpression suppressed the activation of this pathway. In conclusion, we demonstrate that IKKi deficiency exacerbates cardiac hypertrophy by regulating the AKT and NF-κB signaling pathway.
Authors:
Jia Dai; Di-Fei Shen; Zhou-Yan Bian; Heng Zhou; Hua-Wen Gan; Jing Zong; Wei Deng; Yuan Yuan; FangFang Li; Qing-Qing Wu; Lu Gao; Rui Zhang; Zhen-Guo Ma; Hong-Liang Li; Qi-Zhu Tang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-01-22
Journal Detail:
Title:  PloS one     Volume:  8     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2013  
Date Detail:
Created Date:  2013-01-25     Completed Date:  2013-07-09     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e53412     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Cardiomegaly / enzymology*,  pathology,  physiopathology*
Fibrosis
Forkhead Transcription Factors / metabolism
Gene Expression Regulation, Enzymologic / genetics
Gene Knockout Techniques
Glycogen Synthase Kinase 3 / metabolism
Heart / physiopathology
Hemodynamics*
I-kappa B Kinase / deficiency*,  genetics
Male
Mice
Mice, Inbred C57BL
Myocytes, Cardiac / pathology
Proto-Oncogene Proteins c-akt / metabolism
Signal Transduction
TOR Serine-Threonine Kinases / metabolism
Chemical
Reg. No./Substance:
0/Forkhead Transcription Factors; 0/Foxo1 protein, mouse; EC 2.7.1.1/TOR Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.10/I-kappa B Kinase; EC 2.7.11.26/Glycogen Synthase Kinase 3
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