title: 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.affiliation: Department Anatomy and Anthropology, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. rubovitc@post.tau.ac.il
authors.forename: Vardit
authors.initials: V
authors.lastname: Rubovitch
authors.forename: Adi
authors.initials: A
authors.lastname: Shachar
authors.forename: Haim
authors.initials: H
authors.lastname: Werner
authors.forename: Chaim G
authors.initials: CG
authors.lastname: Pick
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D000091342:Endoplasmic Reticulum Chaperone BiP; D007334:Insulin-Like Growth Factor I / Q000008:administration & dosage*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; C000717248:Hspa5 protein, mouse; D007334:Insulin-Like Growth Factor I