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000294721 1001_ $$00000-0001-8268-2671$$aKhan, Dilaware$$b0
000294721 245__ $$aTlx Promotes Stroke-Induced Neurogenesis and Neuronal Repair in Young and Aged Mice.
000294721 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2024
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000294721 520__ $$aStroke is one of the leading causes of chronic disability in humans. It has been proposed that the endogenous neural stem/progenitor cells generate new neurons in the damaged area. Still, the contribution of these cells is negligible because a low number of newborn mature neurons are formed. Tlx conventional knock-out mice, Tlx-CreERT2 mice, and Tlx-overexpressing (Tlx-OE) mice were specifically chosen for their unique genetic characteristics, which were crucial for the experiments. Permanent and transient middle cerebral artery occlusion was used to induce stroke in the mice. Immunostainings for doublecortin and GFP/BrdU/NeuN were performed to study neurogenesis and fate mapping. The rotarod test was performed to assess motor deficits. Here, we show that stroke-induced neurogenesis is dramatically increased with the additional expression of two copies of the nuclear receptor-coding gene tailless (Tlx, also known as Nr2e1), which has been shown to be a master regulator of subventricular zone (SVZ) neural stem cells (NSCs). We show that Tlx expression is upregulated after stroke, and stroke-induced neurogenesis is blocked when Tlx is inactivated. Tlx overexpression in NSCs leads to massive induction of neurogenesis via stroke. More newborn mature neurons are formed in Tlx-overexpressing mice, leading to improved coordination and motor function recovery. Most importantly, we also demonstrate that this process is sustained in aged mice, where stroke-induced neurogenesis is nearly undetectable in wild-type animals. This study provides the first stem cell-specific genetic evidence that endogenous NSCs can be exploited by manipulating their master regulator, Tlx, and thus suggests a novel therapeutic strategy for neuronal repair.
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000294721 650_7 $$2Other$$aTlx
000294721 650_7 $$2Other$$aadult neurogenesis
000294721 650_7 $$2Other$$aneural stem cells
000294721 650_7 $$2Other$$astroke
000294721 650_7 $$2NLM Chemicals$$aNr2e1 protein, mouse
000294721 650_7 $$2NLM Chemicals$$aReceptors, Cytoplasmic and Nuclear
000294721 650_2 $$2MeSH$$aAnimals
000294721 650_2 $$2MeSH$$aNeurogenesis
000294721 650_2 $$2MeSH$$aMice
000294721 650_2 $$2MeSH$$aNeural Stem Cells: metabolism
000294721 650_2 $$2MeSH$$aNeural Stem Cells: cytology
000294721 650_2 $$2MeSH$$aStroke: metabolism
000294721 650_2 $$2MeSH$$aStroke: pathology
000294721 650_2 $$2MeSH$$aNeurons: metabolism
000294721 650_2 $$2MeSH$$aReceptors, Cytoplasmic and Nuclear: metabolism
000294721 650_2 $$2MeSH$$aReceptors, Cytoplasmic and Nuclear: genetics
000294721 650_2 $$2MeSH$$aAging: metabolism
000294721 650_2 $$2MeSH$$aMice, Knockout
000294721 650_2 $$2MeSH$$aMale
000294721 650_2 $$2MeSH$$aMice, Inbred C57BL
000294721 650_2 $$2MeSH$$aInfarction, Middle Cerebral Artery: metabolism
000294721 650_2 $$2MeSH$$aInfarction, Middle Cerebral Artery: pathology
000294721 7001_ $$0P:(DE-He78)5caa069445d78479a7ceae926328e5d8$$aBock, Dagmar$$b1$$udkfz
000294721 7001_ $$0P:(DE-He78)76aeb2431f7458c9261e69c5420390c6$$aLiu, Hai-Kun$$b2$$udkfz
000294721 7001_ $$aMuhammad, Sajjad$$b3
000294721 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms252212440$$gVol. 25, no. 22, p. 12440 -$$n22$$p12440$$tInternational journal of molecular sciences$$v25$$x1422-0067$$y2024
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