Stem cell factor stimulates neurogenesis in vitro and in vivo.
Stem cell factor stimulates neurogenesis in vitro and in vivo.
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DOI：
10.1172/jci15251
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发表时间：
2002-08
期刊：
影响因子：
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通讯作者：
K. Jin;X. Mao;Yunjuan Sun;Lin Xie;D. Greenberg
中科院分区：
文献类型：
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作者：
K. Jin;X. Mao;Yunjuan Sun;Lin Xie;D. Greenberg
脑缺血刺激啮齿动物前脑增殖区的神经发生。为了确定参与的信号因子，从胚胎小鼠大脑中制备的大脑皮层培养物被剥夺了氧气。缺氧增加溴脱氧尿苷（BrdU）掺入细胞表达增殖标记物和未成熟的神经元标记物，缺乏DNA损伤或caspase-3激活的证据。低氧条件培养基和干细胞因子（SCF），这是目前在低氧条件培养基中的水平增加，也刺激BrdU纳入常氧培养。SCF受体，c-kit，表达在神经元培养和成年大鼠大脑的神经增殖区，并在体内给药的SCF增加BrdU标记的未成熟的神经元在这些地区。脑缺氧和缺血可通过包括SCF在内的营养因子刺激神经发生。
Cerebral ischemia stimulates neurogenesis in proliferative zones of the rodent forebrain. To identify the signaling factors involved, cerebral cortical cultures prepared from embryonic mouse brains were deprived of oxygen. Hypoxia increased bromodeoxyuridine (BrdU) incorporation into cells that expressed proliferation markers and immature neuronal markers and that lacked evidence of DNA damage or caspase-3 activation. Hypoxia-conditioned medium and stem cell factor (SCF), which was present in hypoxia-conditioned medium at increased levels, also stimulated BrdU incorporation into normoxic cultures. The SCF receptor, c-kit, was expressed in neuronal cultures and in neuroproliferative zones of the adult rat brain, and in vivo administration of SCF increased BrdU labeling of immature neurons in these regions. Cerebral hypoxia and ischemia may stimulate neurogenesis through trophic factors, including SCF.