期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 354, 期 2, 页码 552-558出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.01.030
关键词
interleukins; myocardial hypertrophy; Akt; signal transduction; mouse; pressure overload
资金
- NHLBI NIH HHS [R21 HL079926, HL68020, R01 HL068020, HL077926] Funding Source: Medline
- NIA NIH HHS [T32 AG021890] Funding Source: Medline
- NIDDK NIH HHS [R01 DK079195] Funding Source: Medline
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 C57B1/6 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 TL-18 plays a critical role in the hypertrophic response. (c) 2007 Elsevier Inc. All rights reserved.
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