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

Vardit Rubovitch*, Adi Shachar, Haim Werner, Chaim G. Pick

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)443-446
Number of pages4
JournalNeurochemistry International
Volume58
Issue number4
DOIs
StatePublished - Mar 2011

Keywords

  • Brain-trauma
  • Cell death mechanisms
  • Cognitive impairments
  • Neuroprotection

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