Matsuoka I, Nakane A, Kurihara K
Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Brain Res. 1997 Nov 21;776(1-2):170-80. doi: 10.1016/s0006-8993(97)01015-9.
Schwann cell is a cell type that forms myelin sheath and provides trophic supports for neuronal cells by producing neurotrophic factors such as neurotrophins and neurokines in both normal and traumatic situations. It was recently reported that after lesion of sciatic nerve, mRNA for cholinergic differentiation factor (CDF)/leukemia inhibitory factor (LIF) is induced in nonneuronal cells in the nerve. However, the source of LIF-mRNA and the mechanism of LIF-mRNA regulation have remained largely unknown. In the present study, we searched for factors regulating the LIF-mRNA expression in cultured Schwann cells isolated from newborn rat sciatic nerve. Among various growth factors and cytokines tested, TGF beta-1 exerted the most prominent effect on the induction of LIF-mRNA in the cultured Schwann cells. The effect of TGF-beta 1 on the increase of LIF-mRNA levels was suppressed by either staurosporine or H-7 suggesting the role of PKC or PKC-like protein kinase activity in the induction of LIF-mRNA. The induction of LIF mRNA by TGF-beta 1 was suppressed in the co-culture of the Schwann cells with embryonic rat DRG neurons. The addition of ascorbic acid, which is known to promote myelination in this co-culture system, further suppressed the TGF-beta 1 induction of LIF-mRNA. These results suggest that Schwann cells respond to TGF-beta 1 in a lesion situation to produce LIF, which supports neuronal survival and regeneration. The re-establishment of neuron-Schwann cell interaction would in turn suppress the LIF production to terminate its action during the lesion situation.
雪旺细胞是一种在正常和创伤情况下形成髓鞘并通过产生神经营养因子(如神经营养蛋白和神经激肽)为神经元细胞提供营养支持的细胞类型。最近有报道称,坐骨神经损伤后,神经中的非神经元细胞会诱导产生胆碱能分化因子(CDF)/白血病抑制因子(LIF)的mRNA。然而,LIF-mRNA的来源以及LIF-mRNA的调控机制在很大程度上仍不清楚。在本研究中,我们寻找了从新生大鼠坐骨神经分离的培养雪旺细胞中调节LIF-mRNA表达的因子。在测试的各种生长因子和细胞因子中,TGFβ-1对培养的雪旺细胞中LIF-mRNA的诱导作用最为显著。星形孢菌素或H-7可抑制TGF-β1对LIF-mRNA水平升高的作用,提示蛋白激酶C(PKC)或PKC样蛋白激酶活性在LIF-mRNA的诱导中起作用。在雪旺细胞与胚胎大鼠背根神经节(DRG)神经元的共培养中,TGF-β1对LIF mRNA的诱导作用受到抑制。在这个共培养系统中,已知添加抗坏血酸可促进髓鞘形成,这进一步抑制了TGF-β1对LIF-mRNA的诱导。这些结果表明,在损伤情况下,雪旺细胞对TGF-β1作出反应以产生LIF,LIF支持神经元的存活和再生。神经元-雪旺细胞相互作用的重建反过来会抑制LIF的产生,从而在损伤情况下终止其作用。