Aguirre Adan, Gallo Vittorio
Center for Neuroscience Research, Children's National Medical Center, 111 Michigan Avenue, NW Washington, DC 20010, USA.
Neuron Glia Biol. 2007 Aug;3(3):209-20. doi: 10.1017/S1740925X08000082.
Neural progenitor cells that express the NG2 proteoglycan are present in different regions of the adult mammalian brain where they display distinct morphologies and proliferative rates. In the developing postnatal and adult mouse, NG2(+) cells represent a major cell population of the subventricular zone (SVZ). NG2(+) cells divide in the anterior and lateral region of the SVZ, and are stimulated to proliferate and migrate out of the SVZ by focal demyelination of the corpus callosum (CC). Many NG2(+) cells are labeled by GFP-retrovirus injection into the adult SVZ, demonstrating that NG2(+) cells actively proliferate under physiological conditions and after demyelination. Under normal physiological conditions and after focal demyelination, proliferation of NG2(+) cells is significantly attenuated in wa2 mice, which are characterized by reduced signaling of the epidermal growth factor receptor (EGFR). This results in reduced SVZ-to-lesion migration of NG2(+) cells and oligodendrogenesis in the lesion. Expression of vascular endothelial growth factor (VEGF) and EGFR ligands, such as heparin binding-EGF and transforming growth factor alpha, is upregulated in the SVZ after focal demyelination of the CC. EGF-induced oligodendrogenesis and myelin protein expression in wild-type SVZ cells in culture are significantly attenuated in wa2 SVZ cells. Our results demonstrate that the response of NG2(+) cells in the SVZ and their subsequent differentiation in CC after focal demyelination depend on EGFR signaling.
表达NG2蛋白聚糖的神经祖细胞存在于成年哺乳动物大脑的不同区域,在这些区域它们呈现出不同的形态和增殖速率。在出生后发育的小鼠和成年小鼠中,NG2(+)细胞是脑室下区(SVZ)的主要细胞群体。NG2(+)细胞在SVZ的前部和外侧区域分裂,并通过胼胝体(CC)的局灶性脱髓鞘刺激而增殖并迁移出SVZ。通过向成年SVZ注射绿色荧光蛋白逆转录病毒标记了许多NG2(+)细胞,表明NG2(+)细胞在生理条件下和脱髓鞘后会积极增殖。在正常生理条件下和局灶性脱髓鞘后,NG2(+)细胞的增殖在wa2小鼠中显著减弱,wa2小鼠的特征是表皮生长因子受体(EGFR)信号传导减少。这导致NG2(+)细胞从SVZ向损伤部位的迁移减少以及损伤部位少突胶质细胞生成减少。在CC局灶性脱髓鞘后,血管内皮生长因子(VEGF)和EGFR配体如肝素结合表皮生长因子和转化生长因子α在SVZ中的表达上调。在培养的野生型SVZ细胞中,表皮生长因子诱导的少突胶质细胞生成和髓磷脂蛋白表达在wa2 SVZ细胞中显著减弱。我们的结果表明,局灶性脱髓鞘后SVZ中NG2(+)细胞的反应及其随后在CC中的分化取决于EGFR信号传导。