Calver A R, Hall A C, Yu W P, Walsh F S, Heath J K, Betsholtz C, Richardson W D
MRC Laboratory for Molecular Cell Biology and Department of Biology, University College London, United Kingdom.
Neuron. 1998 May;20(5):869-82. doi: 10.1016/s0896-6273(00)80469-9.
Oligodendrocyte progenitors originate near the floor plate of the spinal cord, then proliferate and migrate throughout the cord before giving rise to oligodendrocytes. Progenitor cell proliferation stops before birth because the cell cycle slows down, linked to an increase in differentiation and death. Experiments with transgenic mice show that platelet-derived growth factor (PDGF) drives progenitor cell division and suggest that slowing of and exit from the cycle reflects a decline in PDGF signaling. Overexpressing PDGF induces hyperproliferation of progenitor cells and excessive, ectopic production of oligodendrocytes. However, the superfluous oligodendrocytes die at an immature stage of differentiation, leaving a normal complement of myelin-forming cells. Therefore, cell survival controls override proliferation controls for determining the final number and distribution of mature oligodendrocytes.
少突胶质前体细胞起源于脊髓底板附近,然后增殖并迁移至整个脊髓,之后分化为少突胶质细胞。出生前祖细胞增殖停止,因为细胞周期减慢,这与分化和死亡增加有关。转基因小鼠实验表明,血小板衍生生长因子(PDGF)驱动祖细胞分裂,并提示细胞周期的减慢和退出反映了PDGF信号的下降。过度表达PDGF会诱导祖细胞过度增殖以及少突胶质细胞的过量异位产生。然而,多余的少突胶质细胞在分化的未成熟阶段死亡,留下正常数量的形成髓鞘的细胞。因此,在决定成熟少突胶质细胞的最终数量和分布时,细胞存活控制优先于增殖控制。