Transcriptional Profiling in Rat Hair Follicles following Simulated Blast Insult – A New Diagnostic Tool for Traumatic Brain Injury


  1. Wang, Y.
  2. Zhang, J.
  3. Carnduff, L.
  4. Norman, G.
  5. Josey, T.
  6. Sawyer, T.W.
  7. Martyniuk, C.J.
  8. Langlois, V.S.
Corporate Authors
Defence Research and Development Canada, Suffield Research Centre, Ralston AB (CAN);Royal Military Coll of Canada, Kingston ONT (CAN);New Brunswick Univ, Fredericton NB (CAN)
With wide adoption of explosive-dependent weaponry during military activities, Blast-induced neurotrauma (BINT)-induced traumatic brain injury (TBI) has become a significant medical issue. Therefore, a robust and accessible biomarker system is in demand for effective and efficient TBI diagnosis. Such systems will also be beneficial to studies of TBI pathology. Here we propose the mammalian hair follicles as a potential candidate. An Advanced Blast Simulator (ABS) was developed to generate shock waves simulating traumatic conditions on brains of rat model. Microarray analysis was performed in hair follicles to identify the gene expression profiles that are associated with shock waves. Gene set enrichment analysis (GSEA) and sub-network enrichment analysis (SNEA) were used to identify cell processes and molecular signaling cascades affected by simulated bomb blasts. Enrichment analyses indicated that genes with altered expression levels were involved in central nervous system (CNS)/peripheral nervous system (PNS) responses as well as signal transduction including Ca2+, K+- transportation-dependent signaling, Toll-Like Receptor (TLR) signaling and Mitogen Activated Protein Kinase (MAPK) signaling cascades. Many of the pathways identified as affected by shock waves in the hair follicles have been previously reported to be TBI responsive in other organs such as brain and blood. The results suggest that the hair follicle has some common TBI responsive molecular signatures to other
blast;traumatic brain injury;neuroprotection;transcription
Report Number
DRDC-RDDC-2015-P058 — External Literature
Date of publication
01 Aug 2015
Number of Pages
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