通过1型胰岛素样生长因子受体的胰岛素样生长因子（IGF）信号传导在髓鞘再生中起重要作用。
Insulin-like growth factor (IGF) signaling through type 1 IGF receptor plays an important role in remyelination.
作者信息
Mason Jeffrey L, Xuan Shouhong, Dragatsis Ioannis, Efstratiadis Argiris, Goldman James E
机构信息
Department of Pathology and The Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA.
出版信息
J Neurosci. 2003 Aug 20;23(20):7710-8. doi: 10.1523/JNEUROSCI.23-20-07710.2003.
Abstract
We examined the role of IGF signaling in the remyelination process by disrupting the gene encoding the type 1 IGF receptor (IGF1R) specifically in the mouse brain by Cre-mediated recombination and then exposing these mutants and normal siblings to cuprizone. This neurotoxicant induces a demyelinating lesion in the corpus callosum that is reversible on termination of the insult. Acute demyelination and oligodendrocyte depletion were the same in mutants and controls, but the mutants did not remyelinate adequately. We observed that oligodendrocyte progenitors did not accumulate, proliferate, or survive within the mutant mice, compared with wild type, indicating that signaling through the IGF1R plays a critical role in remyelination via effects on oligodendrocyte progenitors.
摘要
我们通过Cre介导的重组，特异性地破坏小鼠大脑中编码1型胰岛素样生长因子受体（IGF1R）的基因，然后将这些突变体和正常的同窝小鼠暴露于铜离子载体，以此研究IGF信号通路在髓鞘再生过程中的作用。这种神经毒素会在胼胝体诱导出脱髓鞘损伤，在损伤终止后是可逆的。突变体和对照组的急性脱髓鞘和少突胶质细胞耗竭情况相同，但突变体没有充分地进行髓鞘再生。我们观察到，与野生型相比，少突胶质前体细胞在突变小鼠体内没有积累、增殖或存活，这表明通过IGF1R的信号传导通过对少突胶质前体细胞的作用，在髓鞘再生中起关键作用。
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