单核细胞趋化蛋白-1 对实验性青光眼中小胶质细胞形态变化的调节和神经保护作用。
Modulation of morphological changes of microglia and neuroprotection by monocyte chemoattractant protein-1 in experimental glaucoma.
机构信息
Laboratory of Neurodegenerative Diseases, Department of Anatomy, University of Hong Kong, Pokfulam, Hong Kong, China.
出版信息
Cell Mol Immunol. 2010 Jan;7(1):61-8. doi: 10.1038/cmi.2009.110.
Abstract
Monocyte chemoattractant protein-1 (MCP-1)/CCL2 is a C-C chemokine involved in the activation and recruitment of monocytic cells to injury sites. MCP-1/CCL2 can induce either neuroprotection or neurodestruction in vitro, depending on the experimental model. We aim to use MCP-1/CCL2 as an experimental tool to investigate the morphological changes of microglia when loss of healthy retinal ganglion cells (RGCs) is exacerbated or attenuated in an experimental glaucoma model. While a high concentration (1000 ng) of MCP-1/CCL2 and lipopolysaccharide (LPS)-exacerbated RGC loss, 100 ng MCP-1/CCL2 provided neuroprotection towards RGC. Neuroprotective MCP-1/CCL2 (100 ng) also upregulated insulin-like growth factor-1 (IGF-1) immunoreactivity in the RGCs. The neuroprotective effect of MCP-1/CCL2 was not due to the massive infiltration of microglia/macrophages. Taken together, this is the first report showing that an appropriate amount of MCP-1/CCL2 can protect RGCs in experimental glaucoma.
摘要
单核细胞趋化蛋白-1（MCP-1）/CCL2 是一种 C-C 趋化因子，参与单核细胞向损伤部位的激活和募集。MCP-1/CCL2 可以在体外诱导神经保护或神经破坏，具体取决于实验模型。我们旨在使用 MCP-1/CCL2 作为实验工具，研究实验性青光眼模型中健康的视网膜神经节细胞（RGC）丢失加剧或减弱时小胶质细胞的形态变化。虽然高浓度（1000ng）的 MCP-1/CCL2 和脂多糖（LPS）加剧了 RGC 的丢失，但 100ng 的 MCP-1/CCL2 对 RGC 具有神经保护作用。具有神经保护作用的 MCP-1/CCL2（100ng）还上调了 RGC 中的胰岛素样生长因子-1（IGF-1）免疫反应性。MCP-1/CCL2 的神经保护作用不是由于小胶质细胞/巨噬细胞的大量浸润。总之，这是第一项表明适量的 MCP-1/CCL2 可以在实验性青光眼模型中保护 RGC 的报告。
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