Impact of the renal insufficiency in the in vivo cardiac tissue: contribution of cell apoptosis in cardiac remodeling

• Grant number: 15/15832-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: January 01, 2016
• End date: December 31, 2016
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Marcela Sorelli Carneiro Ramos
• Grantee: Frayli Maltoni Fratoni
• Host Institution: Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil

Abstract

The immune system presents different interrelations with other organs and tissues, such as the heart tissue. This system operates in several ways, particularly through the production and release of pro and anti inflammatory cytokines, which are capable of carrying on a range of biological effects related to cell proliferation and survival. One of the conditions responsible for the mass production of circulating cytokines is the Acute Renal Failure (ARF) or Chronic Renal Failure (IRC). When it occurs, the kidney failure causes the release of inumerous cytokines, which may act locally and / or migrate to other regions or organs such as the heart, modulating trophism and extracellular matrix components. Previous publications of our laboratory demonstrated that systemic inflammatory process induced by ischemia / reperfusion kidney is able to promote cardiac hypertrophy after 15 days of reperfusion, and also that TLR2 and TLR04 receptors are central factors in the viabilization of the hypertrophic process. The cardiac remodeling phenomenon that occurs during the development of cardiac hypertrophy comprises, in general, a balance between the synthesis of new cellular components (myofibrils) and a degradation, also called apoptosis, of cardiac cells. According to these characteristics, this project aims to elucidate whether there is the activation of apoptotic pathways in cardiac hypertrophy model induced by ischemia / reperfusion kidney. The experimental model of cardiac hypertrophy induced via ischemia / reperfusion renal established and characterized in our laboratory will be used as the main model of this project. Components of apoptosis metabolic pathways will be analysed, such as caspase 3 and 9, Bcl-2, Bax and AIF, with subsequent TUNEL assay to evaluate the presence of apoptotic cells in the hypertrophied heart.

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)

TRENTIN-SONODA, MAYRA; FRATONI, FRAYLI MALTONI; DA CRUZ JUNHO, CAROLINA VICTORIA; SILVA, WELLINGTON CAIO; PANICO, KARINE; CARNEIRO-RAMOS, MARCELA SORELLI. Caspase-1 as Molecular Key in Cardiac Remodeling during Cardiorenal Syndrome Type 3 in the Murine Model. CURRENT MOLECULAR MEDICINE, v. 20, n. 1, p. 72-78, 2020. (15/15832-7, 15/19107-5)