Abstract
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.
Original language | English (US) |
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Pages (from-to) | 88-94 |
Number of pages | 7 |
Journal | Journal of Molecular and Cellular Cardiology |
Volume | 49 |
Issue number | 1 |
DOIs | |
State | Published - Jul 2010 |
Keywords
- Compensatory
- COX-2
- Cyclooxygenase
- Hypertrophy
- Transgenic
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine