Does IGF-1 administration after a mild traumatic brain injury in mice activate the adaptive arm of ER stress?

Abstract

Mild traumatic brain injury (mTBI) induces along with cognitive impairments, both cell death and survival pathways. Previously, IGF-1 (Insulin like growth factor 1) administration prevented TBI-induced damage. This study was aimed at testing the effect of mTBI on ER (endoplasmic reticulum) stress activation and looking for a possible interaction between IGF-1 and ER stress pathways. Mice were subjected to a weight drop closed head injury. Western blot analysis revealed that mTBI induced activation of ATF6 (activating transcription factor 6), but not of CHOP or grp78. IGF-1 administration following mTBI did not change ATF6 or grp78 levels, but significantly elevated CHOP. These results suggest that IGF-1 may exert its neuroprotection via PERK/CHOP, the adaptive arm of the unfolded protein response.

• Authors: Vardit Rubovitch, Adi Shachar, Haim Werner, Chaim G Pick
• Journal: Neurochemistry international (Neurochem Int) Vol. 58 Issue 4 Pg. 443-6 (Mar 2011) ISSN: 1872-9754 [Electronic] England
• PMID: 21219958 (Publication Type: Journal Article)
• Copyright: Copyright © 2011 Elsevier Ltd. All rights reserved.

Chemical References

• Endoplasmic Reticulum Chaperone BiP
• Hspa5 protein, mouse
• Insulin-Like Growth Factor I

Topics

• Animals
• Brain Injuries (metabolism)
• Endoplasmic Reticulum (metabolism)
• Endoplasmic Reticulum Chaperone BiP
• Insulin-Like Growth Factor I (administration & dosage)
• Male
• Mice
• Mice, Inbred ICR