Pro-hypertrophic factors present in post-prandial python serum effects on neonatal rat cardiomyocytes


Meeting Abstract

60.3  Tuesday, Jan. 6  Pro-hypertrophic factors present in post-prandial python serum: effects on neonatal rat cardiomyocytes. RIQUELME, C.A.*; MAGIDA, J.; SECOR, S.M.; LEINWAND, L.A.; University of Colorado, Boulder; University of Colorado, Boulder; University of Alabama, Tuscaloosa; University of Colorado, Boulder cecilia.riquelme@colorado.edu

Burmese pythons are infrequent eaters and after a meal a rapid and significant increase in the size of several organs has been demonstrated. The dry mass of hearts of constricting snakes can increase up to 60% within 48 hours after feeding and return to fasted size shortly thereafter. This striking response has led us to investigate the mechanisms that regulate this physiologic cardiac hypertrophy and regression in pythons. We have hypothesized that post-prandial python serum might contain molecule(s) that can trigger the enlargement of the heart. To test this hypothesis, we have cultured neonatal rat ventricular myocytes (NRVMs) in the presence of fasted and post-fed serum and changes in cell size were determined. NRVMs cultured in media supplemented with 2% post-fed python serum are significantly larger in volume compared to fasted serum. The increase in size is comparable to a known pro-hypertrophic agonist factor such as phenylephrine. Currently, we are performing a systematic study to determine a complete set of metabolites present in the post-fed serum. Concomitant with these studies, we have been seeking for genes activated by the python serum in ventricular myocytes. To do so, we performed a microarray analysis of mRNA extracted from non-treated NRVMS and cultured in the presence of fasted, post-fed serum and phenylephrine. Interestingly, genes activated upon post-fed serum treatment do not cluster together with genes regulated by phenylephrine. From those genes, stand out lipid metabolism-related proteins and channels. These studies will provide us valuable knowledge on molecular events that regulate physiologic cardiac growth. This research was supported by AHA 0725732Z and the Hiberna Corp

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