The immune system presents different interfaces among systems and other body tissues, such as heart tissue. In diseases that generate inflammatory condition, the factors released into the bloodstream can reach many more organs, promoting interaction between tissue cells and immune components. It is known that renal insufficiency (RI) is characterized by a systemic inflammatory condition and that can reach the heart tissue leading to a number of changes. Tissue response may be initiated by Toll-like receptors [TLRs - recognizers molecular patterns associated with pathogens (PAMPs) or related damage (DAMPS)], by the complement system (CS) or both responses. In the inflammatory process, the CS C3a component is released in large quantities and binds to C3aR receptor, which we already know that it is influenced by the activation of TLRs induce transcription of inflammatory factors by translocation of nuclear factor kappa B (NF-kB) into the nucleus. This process can be facilitated by protein kinase dependent calcium / calmodulin II delta (CaMKIId) which in assists the activation process and translocation of NF-kB. Recent studies have demonstrated that kinase alternative actions, such as the transcription CS factor B via TLR4 stimulation. Given the above, this project aims to evaluate the participation of CaMKIId and its impact on CS activation through TLR4 pathway in vitro. For this, it is going to be used primary cultures of cardiomyocytes treated with agonists of TLR4 (HSP70 and LPS) combined or not with the blocker of the CAMKIId. It is expected then that the results of this study can contribute to a better understanding in communicating the heart and related inflammatory processes.
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