184 Urotensin ii induces cardiomyocytes hypertrophy via activation of the mapk and camkii signalling pathways

Introduction The normal concentration of circulating Urotensin II (UII) is elevated in heart failure (Ng et al. 2002). UII has been shown to be involved the development of pathological cardiac hypertrophy (Tzanidis et al. 2003). The aim of this study is to investigate the cellular mechanism by which UII results in ventricular hypertrophy. Methodology Adult Rat Ventricular Myocytes (ARVMs) were isolated from male Wistar rats by enzymatic digestion and placed into primary culture. ARVMs were cultured in six wells plate for up 48 hours. To induce hypertrophy, cells were treated with UII (200 nM) or phenylephrine (10 µM), and hypertrophy quantified as Length/Width (L/W) ratio from photomicrographs. Results Cultured AVRMs exposed to either phenylephrine or UII developed hypertrophy in a time-dependent manner, with a significant reduction in L/W ratio after incubation with UII for 24 hours in comparison with control group (4.25±0.06, n=362 vs. 4.45±0.06, n=335) (p Conclusion These data show that the ERK1/2, p38 and CaMKII signalling pathways are involved in the hypertrophic response to UII. I am currently using Western Blot to confirm the involvement of ERK1/2, P38 and CaMKII pathways. References 1Ng LL, Loke I, O’Brien RJ, Squire IB, Davies JE. Circulation 2001;106(23):2877–2880. 2Tzanidis A, Hannan RD, Thomas WG, Onan D, Autelitano DJ, See F, Kelly DJ, Gilbert RE,Krum H. Circulation Research: Journal of the American Heart Association , 203;93(3):246–253.