Specific Roles of JAKs and STAT3 in Functions of Neural Stem Cells and Committed Neuronal Progenitors during Ethanol-Induced Neurodegeneration
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Peculiar roles of JAKs and STAT3 in realization of growth potential of various types of progenitor cells in neural tissue were examined during ethanol-induced neurodegeneration modeled both in vitro and in vivo. During in vitro action of C2H5OH, these signal molecules exerted the opposite effects on mitotic activity of multipotent neural stem cells and committed neural progenitors (the clonogenic PSA-NCAM+ cells). The JAKs and STAT3 inhibitors down-regulated the rate of neural stem cell division (proliferative activity) but up-regulated such activity of the committed neural progenitors. A long-term in vivo exposure of mice to ethanol inversed the roles of JAKs and STAT3 in determination of proliferative status of neural stem cells and eliminated involvement of JAKs in functional control over the committed progenitors of neurons. The data attest to much promise of STAT3 inhibitors in treatment of ethanol-induced CNS diseases as the remedies that stimulate realization of growth potential in multipotent neural stem cells and committed neural progenitors.
Key Wordsethanol-induced neurodegeneration neural stem cells JAKs STAT3 targeted therapy
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