Changes in Adult Neurogenesis after Traumatic Brain Injury - The Role of TGF-Beta Cytokines and the Transcription Factor Runx1
Abstract
Adult traumatic brain injury (TBI) is a common, acquired injury that often results in permanent loss of neurological function. There are currently no standard treatments aimed at preventing neuronal degeneration during the secondary injury phase or to facilitate regeneration of the central nervous system (CNS). Numerous studies indicate that traumatic brain injury (TBI) increases neurogenesis in the forebrain subventricular zone (SVZ) and the hippocampal dentate gyrus (DG). It is possible that these endogenous stem cell populations could be manipulated to provide replacement neurons to facilitate CNS repair and recovery after injury. Transforming growth factor-beta (TGF-beta) superfamily cytokines are important regulators of adult neurogenesis, but their involvement in regulation of neurogenesis after adult brain injury is unclear. We utilized a craniotomy and controlled cortical impact (CCI) model of TBI in the mouse to investigate the hypothesis that TBI would induce changes in the TGF-beta superfamily signaling pathways within the adult neurogenic regions. Through analysis of qPCR array data generated from RNA isolated from the SVZ and DG of adult mouse at different time points after CCI, we identified major changes in expression of genes involved in the TGF-beta, bone morphogenetic (BMP), and activin signaling pathways, which could bear relevance to the endogenous neural stem and progenitor cell (NSPC) response to injury.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 25, 2014
- Accession Number
- AD1127773
Entities
People
- Trevor T. Logan
Organizations
- Uniformed Services University of the Health Sciences