Analysis of the distribution of VDAC-1 in rat hippocampus following neonatal anoxia

• Grant number: 14/17434-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: January 01, 2015
• End date: December 31, 2015
• Field of knowledge: Biological Sciences - Physiology
• Principal Investigator: Silvia Honda Takada
• Grantee: Débora Sterzeck Cardoso
• Host Institution: Centro de Matemática, Computação e Cognição (CMCC). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil
• Associated scholarship(s): 15/01273-6 - Effects of antenatal hypoxia-ischemia on VDAC-1 distribution in cerebral cortex of rabbits, BE.EP.IC

Abstract

Neonatal anoxia is considered a worldwide clinical problem, with great impact on public health due to its severe and permanent sequelae. The brain damage caused by oxygen deprivation is triggered by several simultaneous cascades, making the study of this phenomenon of cell death a very complex event. In this project, we launched an unprecedented proposal to evaluate the effects of neonatal hypoxia in the distribution of VDAC-1 protein present in the mitochondrial membrane involved in processes of cell death and survival, whose role in anoxic injury, once elucidated, can bring possibilities of new therapeutic perspectives. To elicit anoxia, P1 rats will undergo a 25 minute exposure to 100% nitrogen gas at 37 ° C, according to the model previously described in the literature. In timepoints of 6 and 24 hours after anoxia, their brains will be dissected to study the hippocampus using immunohistochemistry technique to VDAC-1 and Western Blotting analysis. Statistical analysis of the preliminary results showed that the protein level of VDAC-1 24 hours after neonatal anoxia presents a 47% decrease compared to the control group (control: 1 ± 0.12; anoxia: 0.53 ± 0.09, p = 0.01), which does not occur within 6 hours of anoxia (control: 1 ± 0.15; anoxia: 1.04 ± 0.15, p = 0.85). The neonatal anoxia in 24 hours timepoint caused a decrease in VDAC-1 protein in the control group, which may be related to mitochondrial degeneration and cell death observed after oxygen deprivation and that could somehow influence the cognitive sequelae resulting from hippocampal dysfunction, such as deficits in memory and learning, common in people who have suffered anoxia at birth.

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

IKEBARA, JULIANE MIDORI; TAKADA, SILVIA HONDA; CARDOSO, DEBORA STERZECK; MORALLES DIAS, NATALIA MYUKI; VICENTE DE CAMPOS, BEATRIZ CROSSIOL; SANCHES BRETHERICK, TALITHA AMANDA; VILAR HIGA, GUILHERME SHIGUETO; AYRES FERRAZ, MARIANA SACRINI; KIHARA, ALEXANDRE HIROAKI. Functional Role of Intracellular Calcium Receptor Inositol 1,4,5-Trisphosphate Type 1 in Rat Hippocampus after Neonatal Anoxia. PLoS One, v. 12, n. 1, JAN 10 2017. (14/15018-5, 14/16711-6, 15/17044-6, 15/19699-0, 15/19657-5, 14/17434-6)