biostudies-literatureUnknown10(6)Liu ZThe molecular mediators underlying the effects of inflammation on neural stem cells (NSCs) are not fully characterized. In this study, we identified <i>Ascl2</i> as a downstream basic helix-loop-helix (bHLH) transcription factor in NSCs following exposure to TNFα. Under normal conditions, <i>Ascl2</i> expression is inhibited at post-transcriptional levels by miR-26a, which targets the 3' untranslated region (UTR) of <i>Ascl2</i>. Upon exposure to TNFα, miR-26a expression is reduced, which leads to up-regulation of <i>Ascl2</i>. Overexpression of <i>Ascl2</i> promotes neuronal differentiation, reduces proliferation, and increases the level of cleaved CASPASE 3 in NSCs, as observed in the <i>in vitro</i> and <i>in ovo</i> experiments. <i>Ascl2</i> may serve in NSCs as a standby factor that readily responds to TNFα, which is often induced in inflammatory situations. In a chronic inflammatory condition with consistent up-regulation of TNFα, overexpression of <i>Ascl2</i> may inhibit neurogenesis as a net result.Aging and disease1207-1220https://www.ebi.ac.uk/biostudies/studies/S-EPMC6844591biostudies-literatureTNFα-induced Up-regulation of <i>Ascl2</i> Affects the Differentiation and Proliferation of Neural Stem Cells.PMC6844591Liu ZJiang KJi XChen ZZhang YAWang XfalseTNFα-induced Up-regulation of <i>Ascl2</i> Affects the Differentiation and Proliferation of Neural Stem Cells.The molecular mediators underlying the effects of inflammation on neural stem cells (NSCs) are not fully characterized. In this study, we identified <i>Ascl2</i> as a downstream basic helix-loop-helix (bHLH) transcription factor in NSCs following exposure to TNFα. Under normal conditions, <i>Ascl2</i> expression is inhibited at post-transcriptional levels by miR-26a, which targets the 3' untranslated region (UTR) of <i>Ascl2</i>. Upon exposure to TNFα, miR-26a expression is reduced, which leads to up-regulation of <i>Ascl2</i>. Overexpression of <i>Ascl2</i> promotes neuronal differentiation, reduces proliferation, and increases the level of cleaved CASPASE 3 in NSCs, as observed in the <i>in vitro</i> and <i>in ovo</i> experiments. <i>Ascl2</i> may serve in NSCs as a standby factor that readily responds to TNFα, which is often induced in inflammatory situations. In a chronic inflammatory condition with consistent up-regulation of TNFα, overexpression of <i>Ascl2</i> may inhibit neurogenesis as a net result.2019-01-01T00:00:00Z2019 Dec2025-06-01T12:40:59.164Z2025-06-01T12:40:59.164ZS-EPMC68445913178833310.14336/AD.2018.1028