| Grant number: | 20/02923-2 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | January 01, 2021 |
| End date: | December 31, 2022 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Marcela Sorelli Carneiro Ramos |
| Grantee: | Imara Caridad Stable Vernier |
| Host Institution: | Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil |
Abstract Cardiovascular disease (CVD) is the main cause of mortality in patients undergoing hemodialysis and represents 45% of deaths. Left ventricular hypertrophy (LVH) is a common pattern of cardiovascular injury in chronic kidney disease that affects up to 75% of individuals when it affects end-stage renal disease. In addition, renal ischemia/reperfusion (I/R) is the major cause of acute kidney injury predisposing to various disorders, including cardiac electrical disturbance. Cardiorenal syndrome (SCR) is a pathophysiological disorder that affects the kidney and heart. Specifically, CRS type-3 is characterized by an acute worsening of renal function leading to cardiac changes. It is now widely accepted that the innate immune system plays an important role both during the initial insult and in the chronic phase of cardiac injury. It is known that the innate immune system works in conjunction with the adaptive immune system. In this case, the macrophages are able to activate T and B lymphocytes. Regulatory T cells secrete TGF which leads the recruitment of anti-inflammatory M2 macrophages in the myocardium. The specific deletion of Ccl-7 production by B cells limits monocyte/macrophage infiltration, collagen deposition and reduces the remodeling rate in the left ventricle. The events mentioned above occur during the initial phase of the injury, but there is no information about the long-term interaction of macrophages with these cell types induced by acute kidney injury and their impact on cardiac tissue. Given the above, the present study has as main objective: To evaluate the population of macrophages and T and B lymphocytes, in the cardiac tissue, after acute kidney injury. For this, the experiments will be performed using flow cytometry as the main technique. The experimental protocol is already standardized in the laboratory and consists of the induction of renal failure by ischemia, using C57/Bl6 mice. After the different reperfusion times, mononuclear cells from peripheral blood and cardiac tissue will be isolated and finally the characterization of macrophage, T and B lymphocyte populations after kidney injury. (AU) | |
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