Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

James T. Colston, William H. Boylston, Marc D. Feldman, Chris P. Jenkinson, Sam D. de la Rosa, Amanda Barton, Rodolfo J. Trevino, Gregory L. Freeman, Bysani Chandrasekar

Research output: Contribution to journalArticlepeer-review

44 Scopus citations


Interleukin (IL)-18 is a cardiotropic proinflammatory cytokine chronically elevated in the serum of patients with cardiac hypertrophy (LVH). The purpose of this study was to examine the role of IL-18 in pressure-overload hypertrophy using wild type (WT) and IL-18 -/- (null) mice. Adult male C57Bl/6 mice underwent transaortic constriction (TAC) for 7 days or sham surgery. Heart weight/body weight ratios showed blunted hypertrophy in IL-18 null TAC mice compared to WT TAC animals. Microarray analyses indicated differential expression of hypertrophy-related genes in WT versus IL-18 nulls. Northern, Western, and EMSA analyses showed Akt and GATA4 were increased in WT but unchanged in IL-18 null mice. Our results demonstrate blunted hypertrophy with reduced expression of contractile-, hypertrophy-, and remodeling-associated genes following pressure overload in IL-18 null mice, and suggest that IL-18 plays a critical role in the hypertrophic response.

Original languageEnglish (US)
Pages (from-to)552-558
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Mar 9 2007


  • Akt
  • Interleukins
  • Mouse
  • Myocardial hypertrophy
  • Pressure overload
  • Signal transduction

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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