Generation and characterization of a microglial cell line, MG5, derived from a p53-deficient mouse
We have established a cell line cloned from primary‐cultured microglia obtained from p53‐deficient mice. The cell line, MG5, could be grown in astrocyte‐conditioned medium and has been maintained for more than a year. MG5 cells are immunocytochemically positive for Mac‐1 and F4/80 antibody and expre...
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Veröffentlicht in: | Glia 1997-11, Vol.21 (3), p.285-298 |
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Zusammenfassung: | We have established a cell line cloned from primary‐cultured microglia obtained from p53‐deficient mice. The cell line, MG5, could be grown in astrocyte‐conditioned medium and has been maintained for more than a year. MG5 cells are immunocytochemically positive for Mac‐1 and F4/80 antibody and express the major histocompatibility complex (MHC) class I antigen, leukocyte function‐associated antigen‐1, leukocyte common antigen, and intercellular adhesion molecular‐1 mRNA. Interferon‐γ enhanced the expression of MHC class II antigen mRNA in MG5 cells. We previously identified a novel calcium‐binding protein, Iba1 (ionized calcium‐binding adapter molecule 1), which is highly and specifically expressed in cultured microglia. Iba1 protein was also immunocytochemically demonstrated in MG5 cells. The cells retained non‐specific esterase activity, 5′‐nucleotidase activity, acid phosphatase activity, and phagocytic ability. Like primary cultured microglia from wild‐type mice, MG5 cells released nitric oxide in response to lipopolysaccharide, and actively proliferated in the presence of mitogenic factors such as macrophage‐colony stimulating factor (M‐CSF), granulocyte/macrophage‐CSF (GM‐CSF), and interleukin‐3 (IL‐3). Tyrosine‐phosphorylation of M‐CSF receptor in MG5 cells was induced by the addition of M‐CSF or astrocyte‐conditioned medium. These findings indicate that MG5 cells preserve the morphological, biochemical, and physiological properties of primary‐cultured microglia well. The MG5 cell line will be a useful tool for studying microglial function. GLIA 21:285–298, 1997. © 1997 Wiley‐Liss, Inc. |
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ISSN: | 0894-1491 1098-1136 |
DOI: | 10.1002/(SICI)1098-1136(199711)21:3<285::AID-GLIA4>3.0.CO;2-4 |