ACTIVATION AND PROLIFERATION OF THE ISOLATED MICROGLIA BY COLONY STIMULATING FACTOR-I AND POSSIBLE INVOLVEMENT OF PROTEIN KINASE-C
ACTIVATION AND PROLIFERATION OF THE ISOLATED MICROGLIA BY COLONY STIMULATING FACTOR-I AND POSSIBLE INVOLVEMENT OF PROTEIN KINASE-C
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DOI：
10.1016/0006-8993(90)90317-5
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发表时间：
1990-02-12
期刊：
影响因子：
2.9
通讯作者：
MARUNOUCHI, T
中科院分区：
文献类型：
--
作者：
SAWADA, M;SUZUMURA, A;MARUNOUCHI, T
Microglia was isolated from primary mixed brain cell culture of normal newborn mice and then cultivated. They were able to be maintained in vitro for 1-2 months, but incorporated little [3H]thymidine under normal culture conditions. When treated with the conditioned medium of L929 mouse fibroblast cells as a crude CSF-1 (mouse macrophage-colony stimulating factor) or purified CSF-1, microglia showed morphological changes and increased in both cell number and [3H]thymidine uptake. In addition, crude CSF-1 increased lysosomal enzyme activity and superoxide anion formation of microglia up to 2 and 3.8 fold as control value, respectively. These effects of CSF-1 were not observed in the purified astrocyte culture. Purified microglia had CSF-1 receptors which were recognized by the anti-CSF-1 receptor antibody that arose from a peptide of a product of proto-oncogene, c-fms. 12-O-Tetradecanoylphorbol-13-acetate (TPA) also increased microglia cell number and their biochemical activities, suggesting the possible involvement of protein kinase C activation. Protein kinase inhibitors, such as staurosporine or H-7, inhibited the effects of both CSF-1 and TPA. These results indicate that microglia may be regulated in its biochemical and proliferation activities by CSF-1 and that this may occur via activation of protein kinase C.
