Liu Bin, Chen Huiyi, Johns Terrance G, Neufeld Arthur H
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Neurosci. 2006 Jul 12;26(28):7532-40. doi: 10.1523/JNEUROSCI.1004-06.2006.
Modulating the behaviors of reactive astrocytes is a potential therapeutic strategy for neurodegenerative diseases. We found that upregulation and activation of the epidermal growth factor receptor (EGFR) occur in astrocytes after different injuries in optic nerves in vivo. Activation of EGFR regulates genes and cellular processes representing most major markers of reactive astrocytes and genes related with glaucomatous optic neuropathy and other neural disorders. These results suggest that activation of EGFR is a common, regulatory pathway that triggers quiescent astrocytes into reactive astrocytes in response to neural injuries in the optic nerve, and perhaps other parts of the CNS. Targeting EGFR activation using an EGFR tyrosine kinase inhibitor prevents the loss of retinal ganglion cells in a model of glaucomatous optic neuropathy. Because these inhibitors are currently used clinically, our results present an approach to reactive astrocytes as a potential new target for the treatment of neurodegenerations.
调节反应性星形胶质细胞的行为是神经退行性疾病的一种潜在治疗策略。我们发现,在体内视神经发生不同损伤后,星形胶质细胞中表皮生长因子受体(EGFR)会出现上调和激活。EGFR的激活调节着代表反应性星形胶质细胞大多数主要标志物的基因和细胞过程,以及与青光眼性视神经病变和其他神经疾病相关的基因。这些结果表明,EGFR的激活是一条常见的调节途径,它能触发静止的星形胶质细胞在视神经以及可能在中枢神经系统的其他部位发生神经损伤时转变为反应性星形胶质细胞。在青光眼性视神经病变模型中,使用EGFR酪氨酸激酶抑制剂靶向EGFR激活可防止视网膜神经节细胞的丢失。由于这些抑制剂目前已在临床上使用,我们的研究结果为将反应性星形胶质细胞作为神经退行性疾病治疗的潜在新靶点提供了一种方法。