PERK activation preserves the viability and function of remyelinating oligodendrocytes in immune-mediated demyelinating diseases.

ABSTRACT: Remyelination occurs in multiple sclerosis (MS) lesions but is generally considered to be insufficient. One of the major challenges in MS research is to understand the causes of remyelination failure and to identify therapeutic targets that promote remyelination. Activation of pancreatic endoplasmic reticulum kinase (PERK) signaling in response to endoplasmic reticulum stress modulates cell viability and function under stressful conditions. There is evidence that PERK is activated in remyelinating oligodendrocytes in demyelinated lesions in both MS and its animal model, experimental autoimmune encephalomyelitis (EAE). In this study, we sought to determine the role of PERK signaling in remyelinating oligodendrocytes in MS and EAE using transgenic mice that allow temporally controlled activa

SUBMITTER: Lin Y 

PROVIDER: S-EPMC3906495 | biostudies-literature | 2014 Feb

REPOSITORIES: biostudies-literature