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The effects of MIF in the NTS upon microglia activation and inflammatory cytokines in SHR

Grant number: 11/20388-8
Support Opportunities:Scholarships abroad - Research Internship - Post-doctor
Effective date (Start): March 01, 2012
Effective date (End): May 31, 2012
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Eduardo Colombari
Grantee:André Henrique Freiria de Oliveira
Supervisor: Colin Sumners
Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
Research place: University of Florida, Gainesville (UF), United States  
Associated to the scholarship:10/09250-1 - Migration inhibitor factor and reactive oxigen species within nucleus tractus solitarius: role on cardiovascular control and hydroelectrolytic balance in SHR, BP.PD


Many studies try to understand the causes for hypertension and the possible treatments for this pathology. The central nervous system seems to have a key role on development and maintenance of hypertension. Nucleus of solitary tract (NTS) is the major brain area to receive afferents from baro and chemoreflex. Recently, it was showed that macrophage migration inhibitory factor (MIF) has an inhibitory intracellular effect upon angiotensin II (ANGII) actions. MIF counterregulates ANGII effects probably by a reactive oxygen species (ROS) scavenger quality. We have shown that MIF over expression in the NTS was able to reduce the blood pressure in spontaneously hypertensive rats (SHR), a model comparable to essential hypertension in humans. We also demonstrated that ROS levels in the NTS was reduced in MIF-over expressed SHR. Recently inflammatory state has been considered important to genesis and maintenance of hypertension, because some studies relate microglia activation and increase in cytokines levels with ROS increase and hypertension. Therefore, the aim of this study is to investigate if MIF over expression in the NTS can alter microglia activation and inflammatory cytokines levels in NTS of SHR. (AU)

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