Novel crosstalk between ERK MAPK and p38 MAPK leads to homocysteine-NMDA receptor-mediated neuronal cell death.

ABSTRACT: Hyperhomocysteinemia is an independent risk factor for both acute and chronic neurological disorders, but little is known about the underlying mechanisms by which elevated homocysteine can promote neuronal cell death. We recently established a role for NMDA receptor-mediated activation of extracellular signal-regulated kinase (ERK)-MAPK in homocysteine-induced neuronal cell death. In this study, we examined the involvement of the stress-induced MAPK, p38 in homocysteine-induced neuronal cell death, and further explored the relationship between the two MAPKs, ERK and p38, in triggering cell death. Homocysteine-mediated NMDA receptor stimulation and subsequent Ca(2+) influx led to a biphasic activation of p38 MAPK characterized by an initial rapid, but transient activation followed by a del

SUBMITTER: Poddar R 

PROVIDER: S-EPMC3557558 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature