Mouse Cardiac-specific Hsp25Gene Deletions Enhanced Myocardial Hypertrophy By Isoproterenol And Its Mechanisms

Object: Hsp27(Hsp25in mice), a kind of small heat shock protein in human,canbe detected in most cells such as cardiomyocytes. Hsp27/Hsp25has significantanti-apoptotic, anti-oxidative stress the role of a large number of studies have shownthat Hsp27/Hsp25have protective effects on heart failure, myocardial ischemia,injury, cardiac hypertrophy, the early we build a cardiac-specific expression of Hsp27mice transgenic lines observed Hsp27gene transferred to mice to drugs andendotoxin-induced cardiac dysfunction has a protective effect. In recently，we buildHsp25gene knockout mice(KO mice) by Cre-Loxp system, and administrateisopropyladrenaline to induce cardiac hypertrophy model, the observation of theHsp25gene deletion is to increase the phenotype of myocardial hypertrophy, andexplored the possible mechanism.Methods: To evaluate our hypothesis,we administrated mice isoproterenol (ISO)for14days. Assessment of myocardial hypertrophy were determined by heart weight/body weight ratio and heart weight/body weight ratio. Cardiac function wasexamined by echocardiography.Histological chage examinated by grossmorphological, ultrastructural electron microscope. In addition, we analyze the degreeof apoptosis by using Western blot，tunel staining.We examined the levels ofactivation of extracellular signal regulated kinase (ERKs).Results: KO mice increased the degree of cardiac hypertrophy afteradministrating ISO,but had no significant effect on cardiac function. ISOadministration significantly increased cardiac myofilament thick, mitochondrial crest loose of KO mice. Bax/Bcl-2ratio, tunnel staining indicates the degree ofmyocardial apoptosis was significantly increased.ISO also increased the levels ofERKs KO mice compared with WT mice.Conclusion: These results suggest that the Hsp25gene deletion can increase theISO-induced myocardial hypertrophy and that mechanisms may involve increasingapoptosis, activation of ERKs levels.