Modulatory effect of leucine in H9c2 cardiomioblasts under Walker-256 tumor factors

• Grant number: 19/19779-4
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: January 01, 2020
• End date: September 30, 2020
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Maria Cristina Cintra Gomes Marcondes
• Grantee: Maiara Caroline Colombera
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 17/02739-4 - Nutrition and cancer: study of molecular, proteomic and metabolomic aspects of experimental model of cachexia, AP.TEM

Abstract

The mechanism of protein catabolism in the skeletal muscle has been widely studied, especially that induced by a proteolysis-inducing factor (PIF; or even by Walker Factor), as occurred in human and experimental animal tumours. These studies include the cellular signaling processes and metabolic pathways involved mainly in the process of cachexia. In our previous studies we observed that protein degradation is increased and protein synthesis decreased in C2C12 my tubes exposed to Walker factor (FW). Besides, the effects of FW in my tubes are modulated in the presence of leucine, which plays an essential role as metabolic fuel for skeletal muscle, and in stimulating synthesis and inhibiting protein degradation in experimental models of cachexia. Thus, considering the nutritional factors involved in the signaling pathways and also alterations of cellular protein metabolism, It is necessary to investigate the cell proliferation/death, protein degradation and oxidative stress produced during cancer, in order to elucidate key points of the cachexia process, especially in cardiac tissue. Thus, the present project aims to evaluate the modulatory effects of leucine supplementation in cardio myoblasts H9c2 (in vitro model), under the effects of ascites fluid (LA) mimicking the Walker-256 tumour evolution, analysing the cell proliferation death, protein degradation and oxidative stress, comparing these analyses with results previously found in tumour-bearing rats. (AU)