Sun Y, Landis S C, Zigmond R E
Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4975, USA.
Mol Cell Neurosci. 1996 Feb;7(2):152-63. doi: 10.1006/mcne.1996.0012.
Leukemia inhibitory factor (LIF) plays an important role in regulating neuropeptide expression in sympathetic and sensory neurons after axonal transection. By 2 h after axotomy, LIF mRNA increased in nonneuronal cells in sympathetic ganglia and peripheral nerve. In addition, within 1 h of explanting sympathetic ganglia or segments of sympathetic nerve trunks, a protein factor(s) that was able to induce LIF mRNA both in sympathetic cultures and in intact ganglia in vivo was released. This factor(s) appeared to be present in sympathetic ganglia and their nerve trunks under normal conditions and to be activated and/or released after axonal injury. Since the factor(s) has a molecular weight(s) greater than 66 kDa, and no other proteins of such high molecular weight have been previously identified with LIF-inducing activity, it appears to be a novel inducer of LIF.
白血病抑制因子（LIF）在轴突横断后调节交感神经元和感觉神经元中的神经肽表达方面发挥着重要作用。轴突切断后2小时，交感神经节和周围神经的非神经元细胞中LIF mRNA增加。此外，在移出交感神经节或交感神经干节段后的1小时内，一种能够在交感神经培养物和完整神经节体内诱导LIF mRNA的蛋白质因子被释放。该因子在正常情况下似乎存在于交感神经节及其神经干中，并在轴突损伤后被激活和/或释放。由于该因子的分子量大于66 kDa，且之前未鉴定出具有LIF诱导活性的其他如此高分子量的蛋白质，因此它似乎是一种新型的LIF诱导剂。
