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

John M. Streicher, Kenichiro Kamei, Tomo o. Ishikawa, Harvey Herschman, Yibin Wang

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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 languageEnglish (US)
Pages (from-to)88-94
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Issue number1
StatePublished - Jul 2010
Externally publishedYes


  • COX-2
  • Compensatory
  • Cyclooxygenase
  • Hypertrophy
  • Transgenic

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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