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

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.