Leukemia inhibitory factor is an autocrine survival factor for Schwann cells
Leukemia inhibitory factor is an autocrine survival factor for Schwann cells
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DOI：
10.1046/j.1471-4159.1999.0730096.x
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发表时间：
1999-07-01
影响因子：
4.7
通讯作者：
Kilpatrick, TJ
中科院分区：
文献类型：
--
作者：
Dowsing, BJ;Morrison, WA;Kilpatrick, TJ
雪旺细胞在促进神经损伤后的存活和再生中起主要作用。它们的活性包括提供神经营养因子和增加细胞外基质成分和细胞表面粘附分子的产生以促进轴突再生。神经切断后，损伤部位的雪旺细胞上调白血病抑制因子（LIF）。LIF受体在神经损伤部位也上调，但其细胞定位和功能尚未完全表征。我们证明，雪旺细胞表达LIF和LIF受体成分LIF受体β亚基和糖蛋白130的mRNA在体外。我们还表明，虽然LIF是不需要的雪旺氏细胞的发生，它可以加强的背景下neuregulin支持分化的雪旺氏细胞的生存。不仅外源性LIF促进在这些条件下的存活，而且可溶性LIF受体（LIF结合蛋白）和抗LIF抗体的添加显著降低细胞存活，表明LIF发挥自分泌作用。这些结果表明，神经损伤后的雪旺细胞存活可能是由LIF调制。
Schwann cells play a major role in promoting nerve survival and regeneration after injury. Their activities include providing neurotrophic factors and increasing the production of extracellular matrix components and cell surface adhesion molecules to promote axon regeneration. Following nerve transection, leukemia inhibitory factor (LIF) is up-regulated by Schwann cells at the injury site. LIF receptors are also up-regulated at the nerve injury site, but their cellular localization and function have not been fully characterized. We demonstrate that Schwann cells express mRNAs for LIF and the LIF receptor components LIF receptor subunit beta and glycoprotein 130 in vitro. We also show that although LIF is not required for the genesis of Schwann cells, it can potentiate the survival of differentiated Schwann cells in the context of neuregulin support. Not only does exogenous LIF promote survival under these conditions, but addition of the soluble LIF receptor (LIF binding protein) and anti-LIF antibodies significantly reduced cell survival, suggesting that LIF exerts autocrine effects. These results suggest that Schwann cell survival following nerve injury is potentially modulated by LIF.