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

Colston JT, Boylston WH, Feldman MD, Jenkinson CP, de la Rosa SD, Barton A, Trevino RJ, Freeman GL, Chandrasekar B

South Texas Veterans Health Care System, San Antonio, TX, USA.

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 7days 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.

Published 2 February 2007 in Biochem Biophys Res Commun, 354(2): 552-8.
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