PML regulates neuroprotective innate immunity and neuroblast commitment in a hypoxic-ischemic encephalopathy model.

ABSTRACT: Regulation of innate immune responses and activation of tissue regenerative processes are key elements in the pathophysiology of brain injuries. The promyelocytic leukemia (PML) gene was originally identified on a breakpoint of chromosomal translocation t(15;17) associated with acute PML. We have studied the role of PML protein during acute and regenerative phases after hypoxia-ischemia (HI) in brains of neonatal mice. We found that PML prevents tissue loss and apoptotic cell death selectively in subcortical regions of the brain at early stages after damage. In accordance with this, we revealed that PML is important for microglia activation and production of key inflammatory cytokines such as IL1α, IL1β, IL1RN, CXCL10, CCL12 and TNFα. During the regenerative phase, PML-depleted mice were f

SUBMITTER: Palibrk V 

PROVIDER: S-EPMC4973360 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature