The role of erythropoietin upon myocardial fibrosis

• Grant number: 10/06834-2
• Support Opportunities: Regular Research Grants
• Duration: August 01, 2010 - January 31, 2013
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Felix José Alvarez Ramires
• Grantee: Felix José Alvarez Ramires
• Host Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil

Abstract

Regarding the process of myocardial remodeling, secondary to myocardial infarction, we may observe the thinning of the ventricular wall in infarcted area, hypertrophy of the remote area and fibrosis in both areas, showing an overall process of structural and geometric remodeling of the heart. Erythropoietin (EPO), a glycoprotein of 30.4 kDa, has been studied as a cardioprotective peptide, including anti-apoptosis, anti-inflammation and angiogenesis' mediator. The aim of this study was to assess the role of EPO regarding attenuation of structural, geometric and functional remodeling on myocardial infarction model. It will be achieved analyzing the accumulation of interstitial and perivascular collagen, inflammation, oxidative stress and apoptosis. We also will correlate the inflammation, oxidative stress and apoptosis with collagen accumulation and myocardial function. 75 rats will be studied and divided into 5 groups (Control, Control+EPO, Sham, Infarcted, Infarcted+EPO). The methods to be used are: histology for morphometric analysis, RT-real time PCR for inflammation, immunohistochemistry for angiogenisis, echocardiogram for anatomy and myocardial function and ELISA for assessment of oxidative stress. Using the results obtained in this study we will be able to confirm the real protection of EPO on myocardial fibrosis based on the collagen accumulation in the interstitial and perivascular space in the infarcted and particularly in the remote area. Furthermore, we also will be able to analyze the correlation between myocardial fibrosis and function with inflammation, oxidative stress and apoptosis and the role of EPO on it. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

PESSOA, FERNANDA GALLINARO; MADY, CHARLES; BARBOSA FONSECA, KEILA CARDOSO; DE OLIVEIRA-FONOFF, ADRIANA MORGAN; CURY SALEMI, VERA MARIA; JORDAO, MAURICIO RODRIGUES; FERNANDES, FABIO; ALVAREZ RAMIRES, FELIX JOSE. Erythropoietin reduces collagen deposition after myocardial infarction but does not improve cardiac function. Canadian Journal of Physiology and Pharmacology, v. 96, n. 6, p. 541-549, JUN 2018. (10/06834-2)