Document Detail

Compensatory hypertrophy induced by ventricular cardiomyocyte-specific COX-2 expression in mice.
MedLine Citation:
PMID:  20170663     Owner:  NLM     Status:  MEDLINE    
Cyclooxygenase-2 (COX-2) is an important mediator of inflammation in stress and disease states. Recent attention has focused on the role of COX-2 in human heart failure and diseases owing to the finding that highly specific COX-2 inhibitors (i.e., Vioxx) increased the risk of myocardial infarction and stroke in chronic users. However, the specific impact of COX-2 expression in the intact heart remains to be determined. We report here the development of a transgenic mouse model, using a loxP-Cre approach, which displays robust COX-2 overexpression and subsequent prostaglandin synthesis specifically in ventricular myocytes. Histological, functional, and molecular analyses showed that ventricular myocyte specific COX-2 overexpression led to cardiac hypertrophy and fetal gene marker activation, but with preserved cardiac function. Therefore, specific induction of COX-2 and prostaglandin in vivo is sufficient to induce compensated hypertrophy and molecular remodeling.
John M Streicher; Kenichiro Kamei; Tomo-o Ishikawa; Harvey Herschman; Yibin Wang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-02-17
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  49     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-10     Completed Date:  2010-09-10     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  88-94     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Ltd. All rights reserved.
Department of Anesthesiology, David Geffen School of Medicine, University of California - Los Angeles, Los Angeles, CA 90095, USA.
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MeSH Terms
Cardiomegaly / metabolism,  pathology
Cyclooxygenase 2 / metabolism
Cyclooxygenase 2 Inhibitors / metabolism
Heart Failure / metabolism,  pathology,  physiopathology
Heart Ventricles / pathology,  physiopathology*
Hypertrophy / metabolism,  pathology,  physiopathology
Mice, Transgenic
Myocardial Infarction / metabolism,  pathology,  physiopathology
Myocytes, Cardiac / metabolism*,  pathology
Grant Support
CA084572/CA/NCI NIH HHS; HL62311/HL/NHLBI NIH HHS; HL70079/HL/NHLBI NIH HHS; P01 HL080111-050003/HL/NHLBI NIH HHS; R01 HL062311-05/HL/NHLBI NIH HHS; R01 HL062311-09/HL/NHLBI NIH HHS; R01 HL070079-10/HL/NHLBI NIH HHS; R01 HL103205-03/HL/NHLBI NIH HHS; R01 HL108186-02/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Cyclooxygenase 2 Inhibitors; 0/Lactones; 0/Sulfones; 0/rofecoxib; EC 2; EC protein, human

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