Compensatory hypertrophy induced by ventricular cardiomyocyte-specific COX-2 expression in mice.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Streicher, JM; Kamei, K; Ishikawa, T-O; Herschman, H; Wang, Y

Published Date

  • July 2010

Published In

Volume / Issue

  • 49 / 1

Start / End Page

  • 88 - 94

PubMed ID

  • 20170663

Pubmed Central ID

  • PMC2883637

Electronic International Standard Serial Number (EISSN)

  • 1095-8584

Digital Object Identifier (DOI)

  • 10.1016/j.yjmcc.2010.01.021


  • eng

Conference Location

  • England