Down-regulation of MIF by NFκB under hypoxia accelerated neuronal loss during stroke.

Neuronal apoptosis is one of the major causes of poststroke neurological deficits. Inflammation during the acute phase of stroke results in nuclear translocation of NFκB in affected cells in the infarct area. Macrophage migration inhibitory factor (MIF) promotes cardiomyocyte survival in mice following heart ischemia.

Hypoxia signaling regulates macrophage migration inhibitory factor (MIF) expression in stroke.

The macrophage migration inhibitory factor (MIF) is a multifaceted cytokine involved in many processes, including cellular responses to ischemia/reperfusion injury in the heart and brain. This study was undertaken to determine whether human MIF expression is induced following cerebral ischemia and its role therein. To examine whether the induction of MIF gene expression was mediated by its transcriptional upregulation, the human MIF gene promoter was cloned and a luciferase assay was used to determine the presence of a hypoxia-responsive region in the human MIF promoter.

Upregulation of macrophage migration inhibitory factor gene expression in stroke.

Background And Purpose: MIF has been implicated to function in many inflammatory processes. This study examined whether MIF expression was affected in stroke and its underlying molecular mechanism.

Methods: ELISA and qRT-PCR were used to detect MIF protein and mRNA in PBMCs from stroke patients, the ischemic rat brains, and controls.

SP1 regulates a human SNAP-25 gene expression.

The synaptosomal-associated protein of 25 kDa (SNAP-25) is a pre-synaptic plasma membrane protein. SNAP-25 plays an important role in synaptic vesicle membrane docking and fusion, which is involved in the regulation of neurotransmitter release. SNAP-25 has been implicated in the pathogenesis of neuropsychiatric disorders including Schizophrenia, attention-deficit hyperactivity disorder and Alzheimer's disease.