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Effects of antenatal hypoxia-ischemia on VDAC-1 distribution in cerebral cortex of rabbits

Grant number: 15/01273-6
Support Opportunities:Scholarships abroad - Research Internship - Scientific Initiation
Effective date (Start): June 22, 2015
Effective date (End): August 21, 2015
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Silvia Honda Takada
Grantee:Débora Sterzeck Cardoso
Supervisor: Sidhartha Tan
Host Institution: Centro de Matemática, Computação e Cognição (CMCC). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil
Research place: NorthShore University HealthSystem, United States  
Associated to the scholarship:14/17434-6 - Analysis of the distribution of VDAC-1 in rat hippocampus following neonatal anoxia, BP.IC


Hypoxia-ischemia can lead to serious and long lasting consequences and is one of the major causes of brain injury in neonates. Cerebral palsy, one of the most important sequelae of hypoxia-ischemia, has a high incidence that deserves special attention. The difficulty in finding a proper animal model that mimics cerebral palsy is a limiting factor for better understanding this condition. In order to better assess and understand the neuronal injury that can lead to continuous cell loss in cerebral palsy, in this project a rabbit model of cerebral palsy will be employed. The objective of this project is to evaluate possible alterations in VDAC-1's distribution in cerebral cortex of rabbits after antenatal hypoxia-ischemia for a better comprehension of their function on neuronal death. VDAC-1 is a mitochondrial voltage-dependent anion channel that regulates the metabolic influx between the mitochondria and the cytosol. There are evidences showing the fundamental role of VDAC on the release of proapoptotic proteins in the intermembrane space of mitochondria. For this reason, we suggest that this porine may play an important role in neuronal cell death following hypoxia-ischemia. (AU)

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