CETP influence on endothelial function and myocardial infarction: possible relation with mitochondrial function

• Grant number: 19/13862-7
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Start date: August 01, 2019
• End date: July 31, 2024
• Field of knowledge: Biological Sciences - Biochemistry - Metabolism and Bioenergetics
• Principal Investigator: Helena Coutinho Franco de Oliveira
• Grantee: Carolina Martins Lazaro
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 17/17728-8 - Mitochondrial function and dysfunction: implications for aging and associated diseases, AP.TEM

Abstract

Cholesteryl Ester Transfer Protein (CETP) promotes cholesterol transfer from the HDL fraction to lipoproteins containing apolipoprotein B. By reducing HDL, CETP is considered an atherogenic protein. A previous study showed that high plasma concentrations of CETP during the acute phase of myocardial infarction are associated with endothelial dysfunction and increased lethality and recurrence of infarction in the patients studied, possibly due to the reduction of HDL. HDL appears to reduce ischemic damage by protecting against mitochondrial permeability transition in cardiomyocytes. Thus, we intend to study in an experimental model if the CETP superexpression changes 1- endothelium-dependent vascular reactivity in aortas, and 2- the severity of the infarct in vivo and in isolated hearts after ischemia-reperfusion of transgenic mice with CETP vs sibling controls which do not express this protein. We will also characterize the HDL and mitochondrial function of the myocardium in these groups. (AU)