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Contribution of complement system in renal ischemia/reperfusion induced cardiac hypertrophy: role of toll like receptor 4

Grant number: 15/01792-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: June 01, 2015
End date: May 31, 2016
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Marcela Sorelli Carneiro Ramos
Grantee:Carolina Victória da Cruz Junho
Host Institution: Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil

Abstract

The immunological system consists of an array of cells and molecules distributed throughout the organism, its function is to recognize antigens or molecular structures, generating an effective response in the pathogens destruction or inactivation. It can also act via the complement system (CS) which is the primary humoral component of the inflammatory processes. It is well known that cardiac tissue is target of the immunological system and some cardiovascular diseases (CVD) are preceded by general or local inflammation, contributing directly to the remodeling and the heart tropism. It is known that kidney failure may result in the development of systemic inflammation and it can reach the cardiac tissue. The response of the tissue response may be initiated by Toll-like receptors (TLR), which are recognizers pathogen-associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) or also by complement system. During the whole inflammatory process, the complement component C3a is released in abundance and binds to C3aR1 receptor, which is involved in TLRs activation. The objective of this study is to evaluate the role of the complement system in cardiac hypertrophy induced by renal ischemia, and the involvement of TLR 4. For this TLR4 knockout mice will be used as a model of renal ischemia and reperfusion, through the occlusion of the left renal pedicle for 60', followed by reperfusion for 8, 12 or 15 days. It is expected that the results of this study might contribute to a better understanding of the cross-talk between kidney, heart and related inflammatory processes.

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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)
CRUZ JUNHO, V, C.; TRENTIN-SONODA, M.; ALVIM, J. M.; GAISLER-SILVA, F.; CARNEIRO-RAMOS, M. S.. Ca(2+/)Calmodulin-dependent kinase II delta B is essential for cardiomyocyte hypertrophy and complement gene expression after LPS and HSP60 stimulation in vitro. Brazilian Journal of Medical and Biological Research, v. 52, n. 7, . (16/11865-0, 15/19107-5, 15/01792-3, 14/16908-4)
C.V. CRUZ JUNHO; M. TRENTIN-SONODA; J.M. ALVIM; F. GAISLER-SILVA; M.S. CARNEIRO-RAMOS. Ca2+/Calmodulin-dependent kinase II delta B is essential for cardiomyocyte hypertrophy and complement gene expression after LPS and HSP60 stimulation in vitro. Brazilian Journal of Medical and Biological Research, v. 52, n. 7, . (16/11865-0, 15/19107-5, 15/01792-3, 14/16908-4)