The prostaglandin E2 EP2 receptor accelerates disease progression and inflammation in a model of amyotrophic lateral sclerosis.

ABSTRACT:

Objective

Inflammation has emerged as an important factor in disease progression in human and transgenic models of amyotrophic lateral sclerosis (ALS). Recent studies demonstrate that the prostaglandin E(2) EP2 receptor is a major regulator of inflammatory oxidative injury in innate immunity. We tested whether EP2 signaling participated in disease pathogenesis in the G93A superoxide dismutase (SOD) model of familial ALS.

Methods

We examined the phenotype of G93A SOD mice lacking the EP2 receptor and performed immunocytochemistry, quantitative reverse transcriptase polymerase chain reaction, and Western analyses to determine the mechanism of EP2 toxicity in this model.

Results

EP2 receptor is significantly induced in G93A SOD mice in astrocytes and microglia in paralle

SUBMITTER: Liang X 

PROVIDER: S-EPMC2766522 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature