Advanced search
Start date
Betweenand

Investigation of insulin degrading enzyme (IDE) regulatory role in olfactory sensory neurons regeneration

Grant number: 12/21854-5
Support type:Scholarships abroad - Research Internship - Doctorate (Direct)
Effective date (Start): April 01, 2013
Effective date (End): May 31, 2013
Field of knowledge:Biological Sciences - Biochemistry - Molecular Biology
Principal Investigator:Isaias Glezer
Grantee:Umberto Crisafulli
Supervisor abroad: Malcolm Arthur Leissring
Home Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Local de pesquisa : Mayo Clinic, Florida, United States  
Associated to the scholarship:11/13134-0 - Study of the influence of signaling Toll-Like Receptors (TLRs) and the gene MyD88 on olfactry epithelium neuronal regeneration, BP.DD

Abstract

The immune cells are recruited during the regenerative process that takes place after brain injury. The inflammatory reaction associated with this process is essential for pathogen and damaged tissue elimination, as well for tissue recovery. The cells that conduct the innate immune response express Toll-like receptors (TLRs), which transduce signals and induce gene expression following pathogen or injury detection. Our studies suggest that the deletion of Myd88 gene, which encodes an adapter protein for several TLRs and Interleukin-1 beta receptor, accelerates murine Olfactory Epithelium (OE) regeneration. In order to identify genes related with this enhanced neurogenesis, we performed microarray analysis of injured OE, comparing wild-type and Myd88-/- mice. Among the differentially expressed genes, we observed a remarkable change in Ide (Insulin Degrading Enzyme) transcript levels. The aim of this project is to evaluate whether IDE expression changes account for Myd88-/- observed phenotype. In order to fulfill this purpose, we managed a collaborative work to perform IDE enzymatic activity assay in the course of OE regeneration and the analysis of olfactory neurons reappearance after injury in Ide-/- mice. (AU)