RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.

ABSTRACT:

Aims

Neuronal cell death is a primary factor that determines the outcome after traumatic brain injury (TBI). We previously revealed the importance of receptor for activated C kinase (RACK1), a multifunctional scaffold protein, in maintaining neuronal survival after TBI, but the specific mechanism remains unclear. The aim of this study was to explore the mechanism underlying RACK1-mediated neuroprotection in TBI.

Methods

TBI model was established using controlled cortical impact injury in Sprague-Dawley rats. Genetic intervention and pharmacological inhibition of RACK1 and PERK-autophagy signaling were administrated by intracerebroventricular injection. Western blotting, coimmunoprecipitation, transmission electron microscopy, real-time PCR, immunofluorescence, TUNEL staining

SUBMITTER: Ni H 

PROVIDER: S-EPMC10966134 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature