Mitrasinovic Olivera M, Vincent Valerie A M, Simsek Dilek, Murphy Greer M
Neuroscience Research Laboratories, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305-5485, USA.
Neurosci Lett. 2003 Jul 3;344(3):185-8. doi: 10.1016/s0304-3940(03)00474-9.
Macrophage colony stimulating factor (M-CSF) and its receptor are upregulated in the brain in Alzheimer's disease. M-CSF induces activation and proliferation of microglial cells and expression of proinflammatory cytokines. Amyloid beta (Abeta) immunization experiments suggest that microglia have the capacity to aggressively clear Abeta from the brain under certain circumstances. We examined the role of M-CSF in phagocytosis of fluorescent microspheres and Abeta by cultured microglia. M-CSF treatment increased microglial cell phagocytosis of both microspheres and of Abeta. Antibody neutralization of M-CSF inhibited Abeta uptake induced by overexpression of the M-CSF receptor on microglia. These results suggest that M-CSF could be important in promoting microglial clearance of abnormal protein aggregates such as Abeta.
巨噬细胞集落刺激因子(M-CSF)及其受体在阿尔茨海默病患者的大脑中上调。M-CSF可诱导小胶质细胞活化、增殖以及促炎细胞因子的表达。淀粉样β蛋白(Aβ)免疫实验表明,在某些情况下,小胶质细胞有能力从大脑中积极清除Aβ。我们研究了M-CSF在培养的小胶质细胞吞噬荧光微球和Aβ中的作用。M-CSF处理增加了小胶质细胞对微球和Aβ的吞噬作用。对M-CSF进行抗体中和可抑制小胶质细胞上M-CSF受体过表达诱导的Aβ摄取。这些结果表明,M-CSF在促进小胶质细胞清除异常蛋白聚集体(如Aβ)方面可能很重要。