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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Distinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineage.
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Distinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineage.

机译：不同的成纤维细胞生长因子（FGF）/ FGF受体信号对在少突胶质细胞谱系中引发多种细胞应答。

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Fibroblast growth factors (FGFs) have been implicated in numerous cellular processes, including proliferation, migration, differentiation, and survival. Whereas FGF-2, the prototypic ligand in a family of 22 members, activates all four tyrosine kinase FGF receptors (FGFR1-FGFR4), other members demonstrate a higher degree of selectivity. Oligodendrocytes (OLs), the myelin-producing cells of the CNS, are highly influenced by FGF-2 at all stages of their development. However, how other FGFs and their cognate receptors orchestrate the development of OLs is essentially undefined. Using a combination of specific FGF ligands and receptor blocking antibodies, we now show that FGF-8 and FGF-17 target OL progenitors, inhibiting their terminal differentiation via the activation of FGFR3, whereas FGF-9 specifically targets differentiated OLs, triggering increases in process growth via FGFR2 signaling; FGF-18 targets both OL progenitors and OLs via activation of both FGFR2 and FGFR3. These events are highly correlated with changes in FGF receptor expression from FGFR3 to FGFR2 as OL progenitors differentiate into mature OLs. In addition, we demonstrate that, although activation of FGFR1 by FGF-2 leads to proliferation of OL progenitors, it produces deleterious effects on differentiated OLs (i.e., aberrant reentry into cell cycle and down-regulation of myelin proteins with a loss of myelin membrane). These data suggest that ligand availability, coupled with changes in FGF receptor expression, yield a changing repertoire of ligand-receptor signaling complexes that contribute critically to the regulation of both normal OL development and potential OL/myelin pathogenesis.
机译：成纤维细胞生长因子（FGFs）已参与许多细胞过程，包括增殖，迁移，分化和存活。 FGF-2是22个成员家族中的原型配体，可激活所有四个酪氨酸激酶FGF受体（FGFR1-FGFR4），而其他成员则表现出更高的选择性。少突胶质细胞（OLs）是中枢神经系统产生髓磷脂的细胞，在其发育的各个阶段都受到FGF-2的强烈影响。但是，其他FGF及其同源受体如何协调OL的发育基本上还不确定。使用特定的FGF配体和受体阻断抗体的组合，我们现在显示FGF-8和FGF-17靶向OL祖细胞，通过激活FGFR3抑制其终末分化，而FGF-9特异性靶向分化的OL，触发过程增加通过FGFR2信号传导生长; FGF-18通过激活FGFR2和FGFR3同时靶向OL祖细胞和OL。这些事件与OL祖细胞分化为成熟OL时从FGFR3到FGFR2的FGF受体表达变化高度相关。此外，我们证明，尽管FGF-2激活FGFR1导致OL祖细胞增殖，但它对分化的OL产生有害作用（即，异常折返进入细胞周期，并下调髓磷脂蛋白，使髓磷脂膜减少）。 ）。这些数据表明，配体可用性以及FGF受体表达的变化会产生配体-受体信号转导复合物的变化，这对正常OL的发育和潜在的OL /髓鞘发病机理的调节均至关重要。

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