Differing in vitro survival dependency of mouse and rat NG2+ oligodendroglial progenitor cells.
Differing in vitro survival dependency of mouse and rat NG2+ oligodendroglial progenitor cells.
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DOI：
10.1002/jnr.22262
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发表时间：
2010-04
影响因子：
4.2
通讯作者：
Itoh, Takayuki
中科院分区：
文献类型：
--
作者：
Horiuchi, Makoto;Lindsten, Tullia;Pleasure, David;Itoh, Takayuki
关键词：
NG2 硫酸软骨素蛋白多糖是多种物种少突胶质祖细胞 (OPC) 的表面标记物。然而，与充分研究的大鼠 OPC 相比，我们发现纯化的小鼠 NG2 表面阳性细胞（NG2+ 细胞）需要额外激活环 AMP (cAMP) 信号才能在含有 30% B104 神经母细胞瘤条件培养基并补充有成纤维细胞生长因子-2 (B104CM+FGF2) 的培养基中生存，而单独的 B104CM+FGF2 就足以生存，并且 大鼠OPCs的选择性增殖。体外诱导分化后，超过90%的小鼠NG2+细胞变为O4阳性，并且大多数在分化5天时表达髓磷脂碱性蛋白，这证实了分离的小鼠NG2+细胞为OPC的身份。与大鼠 OPC 相比，B104CM+FGF2 中的小鼠 OPC 运动能力较差，并且 ERK1/2 和 cAMP 反应元件结合蛋白 (CREB) 的基础磷酸化水平较低，并且内源性途径介导的细胞凋亡发生率较高。 cAMP-CREB 信号传导的瞬时上调部分抑制了小鼠 OPC 的凋亡，与 ERK 通路无关。这项研究证明了小鼠和大鼠 OPC 之间的营养需求存在差异，cAMP 信号传导在保持小鼠 OPC 的活力方面发挥着重要作用。
NG2 chondroitin sulfate proteoglycan is a surface marker of oligodendroglial progenitor cells (OPCs) in various species. In contrast to well-studied rat OPCs, however, we found that purified mouse NG2 surface positive cells (NG2+ cells) require additional activation of cyclic AMP (cAMP) signaling for survival in a medium containing 30% B104 neuroblastoma conditioned medium supplemented with fibroblast growth factor-2 (B104CM+FGF2), whereas B104CM+FGF2 alone is sufficient for survival and selective proliferation of rat OPCs. After induction of in vitro differentiation, more than 90% of mouse NG2+ cells became O4-positive, and a majority expressed myelin basic protein by 5 day of differentiation, which confirmed the identity of isolated mouse NG2+ cells as OPCs. In comparison to rat OPCs, mouse OPCs in B104CM+FGF2 were less motile, and demonstrated lower basal phosphorylation levels of ERK1/2 and cAMP response element-binding protein (CREB) and a higher incidence of apoptosis mediated by the intrinsic pathway. Transient up-regulation of cAMP-CREB signaling partially inhibited apoptosis of mouse OPCs independently of the ERK pathway. This study demonstrates a difference in trophic requirements between mouse and rat OPCs, with an essential role for cAMP signaling to preserve viability of mouse OPCs.
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