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TLR4 and complement system : possible key mechanism in renal ischemia/reperfusion induced cardiac hypertrophy

Grant number: 15/19107-5
Support type:Regular Research Grants
Duration: February 01, 2016 - June 30, 2018
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:Marcela Sorelli Carneiro Ramos
Grantee:Marcela Sorelli Carneiro Ramos
Home 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 interacts with several different tissues and organs of the human body, for example, the heart tissue. In diseases that generate a systemic inflammation, some factors are released in the blood stream and they are able to reach the most diverse organs, promoting interaction between tissue cells and immunity cells. It is known that renal insufficiency (RI) is characterized by generation of systemic inflammation, whereas it might reach the heart tissue, leading to a series of alterations. The local response can be initiated by receptors named Toll-like [TLRs - recognizers of pathogen-associated molecular patterns (PAMPs) or danger associated molecular patterns (DAMPs)], via complement system or combined responses. During inflammation, the complement system component C3a is released in large amounts and binds to its receptor C3aR1, which is able to assist in the TLRs activation, inducing transcription of inflammatory factors throughout translocation of the nuclear factor kappa B (NF-ºB) to the nucleus. Such process can be facilitated by a kinase named Ca2+/calmodulin-dependent protein kinase type II delta (CaMKII´ which, in turn, helps in the NF-ºB activation and then translocation to the nucleus. Although the majority of studies related to CaMKII´ are directed to its participation in cardiac calcium homeostasis, new studies have been demonstrating alternative actions, such as transcription of complement system factor B via TLR4 stimulation. Based on above considerations, the present work aims to evaluate the interaction between complement system and TLR4 on cardiac hypertrophy development induced by renal ischemia/reperfusion; Therefore, it was be performed procedure of unilateral renal pedicle occlusion during 60 min, followed by reperfusion of 8, 12 or 15 days. Analysis of gene expression reveals altered levels of SC components (from classic and alternative pathways) as well as CaMKII´ suggesting a role of SC in cardiac hypertrophy induced by renal ischemia-reperfusion. (AU)

Scientific publications (4)
(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. Web of Science Citations: 0.
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, p. -, 2019.
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 2019. Web of Science Citations: 1.
CIRINO-SILVA, ROGERIO; KMIT, FERNANDA V.; TRENTIN-SONODA, MAYRA; NAKAMA, KARINA K.; PANICO, KARINE; ALVIM, JULIANA M.; DREYER, THIAGO R.; MARTINHO-SILVA, HERCULANO; CARNEIRO-RAMOS, MARCELA S. Renal ischemia/reperfusion-induced cardiac hypertrophy in mice: Cardiac morphological and morphometric characterization. JRSM CARDIOVASCULAR DISEASE, v. 6, JAN 1 2017. Web of Science Citations: 0.

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