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• W1970792956 abstract "HIF-1α is a hypoxia-inducible protein that regulates many cell and molecular processes, including those involved in angiogenesis and stem cell maintenance. Prior studies demonstrated constitutive HIF-1α stabilization in neural stem cells (NSCs) of the adult mouse SVZ, but its role there has not been elucidated. Here, we tested the hypothesis that HIF-1α plays an essential role in the maintenance of adult NSCs and stabilization of the SVZ vascular niche using conditional, tamoxifen-inducible <i>Hif1a</i> knock-out mice. We generated nestin-CreER^T2/R26R-YFP/<i>Hif1a</i>^fl/fl triple transgenic mice, to enable tamoxifen-inducible <i>Hif1a</i> gene inactivation in nestin-expressing NSCs within the adult SVZ. <i>Hif1a</i> gene deletion resulted in a significant loss of YFP⁺ NSCs within the SVZ by 45 d post recombination, which was preceded by significant regression of the SVZ vasculature at 14 d, and concomitant decrease of VEGF expression by NSCs. Loss of YFP⁺ NSCs following <i>Hif1a</i> gene inactivation <i>in vivo</i> was likely an indirect consequence of vascular regression, since YFP⁺ neurosphere formation over serial passage was unaffected. These results identify NSC-encoded HIF-1α as an essential factor in the maintenance of the adult SVZ, and demonstrate that NSCs within the SVZ maintain the integrity of their vascular niche through HIF-1α-mediated signaling mechanisms." @default.
• W1970792956 created "2016-06-24" @default.
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• W1970792956 date "1995-01-14" @default.
• W1970792956 modified "2023-09-26" @default.
• W1970792956 title "Clonality in Langerhans' cell histiocytosis" @default.
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• W1970792956 doi "https://doi.org/10.1136/bmj.310.6972.74" @default.
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