Ikeda T, Puro D G
Department of Ophthalmology, University of Michigan, W.K. Kellogg Eye Center, Ann Arbor 48105.
Brain Res. 1994 Jun 27;649(1-2):260-4. doi: 10.1016/0006-8993(94)91072-3.
Knowledge of the effects of nerve growth factor (NGF) on glia is limited. A CNS site where NGF-glial interactions may occur is the retina. NGF is endogenous to the retina, and the retinal Müller glial cells have NGF receptors. Here, we examined the possibility that NGF may be a mitogen for Müller glial cells, which often proliferate in response to pathophysiological conditions. Experiments were performed on cultured glial cells from the adult human retina. Exposure of cultured Müller glial cells to 2.5 S NGF under serum-free conditions resulted in a concentration-dependent increase in cell number and bromodeoxyuridine incorporation into nuclei. The half-maximally effective concentration was 0.04 ng/ml (1.5 pM), consistent with activation of high affinity NGF receptors. K252a, a blocker of the neurotrophin family of tyrosine kinase-linked receptors, potently inhibited the proliferative effect of NGF. Transforming growth factor beta-2, another growth factor endogenous to the retina, inhibited the mitogenic response to NGF. These findings indicate that human Müller glial cells in culture express functional NGF receptors and that the response of Müller cells to NGF can be modulated by other growth factors.
关于神经生长因子（NGF）对神经胶质细胞作用的了解有限。视网膜是中枢神经系统中可能发生NGF与神经胶质细胞相互作用的部位。NGF是视网膜内源性的，视网膜穆勒神经胶质细胞具有NGF受体。在此，我们研究了NGF可能是穆勒神经胶质细胞有丝分裂原的可能性，穆勒神经胶质细胞常因病理生理状况而增殖。对来自成年人类视网膜的培养神经胶质细胞进行了实验。在无血清条件下，将培养的穆勒神经胶质细胞暴露于2.5 S NGF中，导致细胞数量和溴脱氧尿苷掺入细胞核的浓度依赖性增加。半数有效浓度为0.04 ng/ml（1.5 pM），与高亲和力NGF受体的激活一致。K252a是酪氨酸激酶连接受体神经营养因子家族的一种阻滞剂，能有效抑制NGF的增殖作用。视网膜内源性的另一种生长因子转化生长因子β-2抑制了对NGF的促有丝分裂反应。这些发现表明，培养的人类穆勒神经胶质细胞表达功能性NGF受体，并且穆勒细胞对NGF的反应可被其他生长因子调节。
