| Compensatory hypertrophy induced by ventricular cardiomyocyte-specific COX-2 expression in mice. | |
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MedLine Citation:
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PMID: 20170663 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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John M Streicher; Kenichiro Kamei; Tomo-o Ishikawa; Harvey Herschman; Yibin Wang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-02-17 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 49 ISSN: 1095-8584 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-06-10 Completed Date: 2010-09-10 Revised Date: 2012-02-20 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 88-94 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Anesthesiology, David Geffen School of Medicine, University of California - Los Angeles, Los Angeles, CA 90095, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cardiomegaly / metabolism, pathology Cyclooxygenase 2 / metabolism Cyclooxygenase 2 Inhibitors / metabolism Heart Failure / metabolism, pathology, physiopathology Heart Ventricles / pathology, physiopathology* Hypertrophy / metabolism, pathology, physiopathology Lactones Mice Mice, Transgenic Myocardial Infarction / metabolism, pathology, physiopathology Myocytes, Cardiac / metabolism*, pathology Sulfones |
| Grant Support | |
ID/Acronym/Agency:
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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 |
| Chemical | |
Reg. No./Substance:
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0/Cyclooxygenase 2 Inhibitors; 0/Lactones; 0/Sulfones; 0/rofecoxib; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/PTGS2 protein, human |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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