Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The suppressor of cytokine signaling 2 (SOCS2) has been reported to be involved in astroglial reactions and adult neurogenesis in the ischemic hippocampus. To elucidate whether SOCS2 is implicated in the pathophysiology of stroke, we investigate spatiotemporal regulation and identification of cell phenotypes expressing SOCS2 after transient focal cerebral ischemia. Weak hybridization signals for SOCS2 mRNA were constitutively observed in striatal neurons and upregulation of SOCS2 mRNA was induced in association with nestin-positive cells in stroke-lesioned rats. Analysis of the characteristics and phenotypes of SOCS2/nestin double-labeled cells revealed spatial differences between infarct and peri-infarct areas. SOCS2/nestin double-labeled cells in the infarct area were associated with the vasculature and were highly proliferative. In contrast, the double-labeled cells in the peri-infarct area were indeed glial fibrillary acidic protein (GFAP)-positive reactive astrocytes forming the glial scar, although nestin-negative reactive astrocytes also exhibited weak SOCS2 expression. In addition, induction of SOCS2 expression was observed in Iba1-positive cells showing a macrophage-like phenotype with amoeboid morphology; these cells were predominantly localized in the infarct area. In the peri-infarct area, only a small proportion of Iba1-positive cells with the morphology of brain macrophages expressed SOCS2 and most activated stellate microglial cells with thick and short processes exhibited weak or negligible SOCS2 expression. Thus, our results revealed the phenotypic and functional heterogeneity of SOCS2-expressing cells within infarct and peri-infarct areas, suggesting the involvement of SOCS2 in astroglial reactions and activation/recruitment of brain macrophages and its potential role in perivascular progenitors/stem cells after ischemic stroke.
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PMID:Expression of SOCS2 mRNA and protein in the ischemic core and penumbra after transient focal cerebral ischemia in rats. 2713 May 72

Suppressor of cytokine signaling 2 (SOCS2) is a well-established negative regulator of growth hormone signaling that acts on adult hippocampal neurogenesis during ischemic insults. To explore whether SCOS2 is involved in poststroke neurogenesis, we studied the temporal expression of SOCS2 mRNA in the subventricular zone (SVZ) of rats after transient focal cerebral ischemia. We found that SOCS2 expression was upregulated in the SVZ of the infarcted hemisphere. The number of SOCS2-expressing cells was significantly increased in the ipsilateral SVZ compared with that on the contralateral side on days 7-10 after reperfusion, and SOCS2-expressing cells were highly proliferative, coinciding both spatially and temporally with stroke-induced neurogenesis. Almost all SOCS2-expressing cells in the SVZ were colabeled with the neural stem cell markers nestin and musashi1 and the neural/glial progenitor transcription factor Sox-2. In addition, SOCS2 was highly expressed in newly generated neurons that were immunoreactive for polysialic acid-neural cell adhesion molecule, indicating that SOCS2 expression may be persistent during neuronal differentiation. Thus, our data demonstrated that SOCS2 mRNA was highly expressed in proliferating neural stem/precursor cells and postmitotic migratory neuroblasts in the SVZ niche after focal cerebral ischemia, suggesting that SOCS2 may be actively involved in regulating adult neurogenesis induced by ischemic stroke.
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PMID:Increased expression of suppressor of cytokine signaling 2 in the subventricular zone after transient focal cerebral ischemia in adult rats. 2747 95