Myocardial gene expression associated with genetic cardiac hypertrophy in the absence of hypertension.

摘要: The hypertrophic heart rat (HHR) was derived from the spontaneously hypertensive of Okamoto strain and develops cardiac hypertrophy in absence hypertension. genetic basis this is unknown. Therefore, we compared gene expression profiles left ventricular myocardium young (8-10 weeks age) old (38-50 weeks) HHR with rats an age-matched control strain, normal (NHR). cDNA microarrays (National Institute Aging [NIA], 15,247 clones) were used to evaluate cardiac-derived Cy3 Cy5 labeled cDNA. M values (log2[Cy5/Cy3]) obtained significant differential identified using empirical Bayesian approach specific results verified real-time PCR. Compared NHR, weight index (heart weight/ body weight) significantly elevated at both ages (young: 5.5 +/- 0.5 vs. 3.9 0.2; old: 4.2 0.3 3.4 0.2 mg/g; p < 0.05) no difference or tail-cuff blood pressure detected between strains either age. Differential observed 65 390 clones HHR, respectively, more genes exhibiting down-regulation than up-regulation instances down 44 up 21; 292 98). Our data suggest a role for Ras/mitogen-activated protein kinase (MAPK) signaling pathway tumor necrosis factor (TNF) receptor-mediated activation nuclear factor-kappaB (NF-kappaB) etiology enlargement HHR. These findings support candidature previously cardiotrophic agents contributing normotensive also identify novel factors which may be involved genesis primary hypertrophy.