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  • Title: JAK2-STAT3 signaling pathway mediates thrombin-induced proinflammatory actions of microglia in vitro.
    Author: Huang C, Ma R, Sun S, Wei G, Fang Y, Liu R, Li G.
    Journal: J Neuroimmunol; 2008 Nov 15; 204(1-2):118-25. PubMed ID: 18710787.
    Abstract:
    The present study shows that JAK2-STAT3 inflammatory signaling mediates thrombin-stimulated microglia activation. In rat primary microglia, thrombin rapidly activated JAK2 and induced phosphorylation of STAT3. In addition, thrombin increased transcription of the inflammation-associated genes tumor necrosis factor (TNF)-alpha, inducible nitric oxide synthase (iNOS), production of TNF-alpha, NO and induced neurodegeneration of dopaminergic neurons in mesencephalic cultures. AG490, a JAK inhibitor, markedly reduced activation of JAK2 and STAT3 in thrombin-treated microglia. AG490 also inhibited thrombin-induced transcription and expression of TNF-alpha, iNOS and/or NO release, moreover rescued dopaminergic neurons. These results suggest that JAK2-STAT3 signaling pathway plays a critical role in mediating thrombin-induced activation of microglia and degeneration of dopaminergic neurons.
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