| Grant number: | 15/19107-5 |
| Support Opportunities: | Regular Research Grants |
| Start date: | February 01, 2016 |
| End date: | June 30, 2018 |
| Field of knowledge: | Biological Sciences - Immunology - Cellular Immunology |
| Principal Investigator: | Marcela Sorelli Carneiro Ramos |
| Grantee: | Marcela Sorelli Carneiro Ramos |
| Host Institution: | Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Santo André , SP, Brazil |
| City of the host institution: | Santo André |
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)
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