Generation and characterization of a microglial cell line, MG5, derived from a p53-deficient mouse

Ohsawa, Keiko; Imai, Yoshinori; Nakajima, Kazuyuki; Kohsaka, Shinichi

doi:10.1002/(sici)1098-1136(199711)21:3<285::aid-glia4>3.0.co;2-4

Cited by 76 publications

(30 citation statements)

References 51 publications

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“…MG20 and MG0 cells were mostly rounded or flattened in shape, but occasionally had a spindle or ramified morphology in culture. These morphological characteristics were similar to those of primary microglia (3) and microglial cell lines (21), including MG6 cells (32). In addition, they actively phagocytosed latex beads and produced inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-1␣, and interleukin-6, when stimulated by lipopolysac-charide (data not shown), indicating that established cell lines possess morphological, physiological, and immunological characteristics of microglia in the mouse brain.…”

supporting

confidence: 58%

Microglial Cell Line Established from Prion Protein-Overexpressing Mice Is Susceptible to Various Murine Prion Strains

Iwamaru

Takenouchi

Ogihara

et al. 2007

J Virol

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Several lines of evidence suggest that microglia have important roles in the pathogenesis of prion diseases. Here, we establish a novel microglial cell line (MG20) from neonatal tga20 mice that overexpress murine prion protein. After exposure to Chandler scrapie, we observed the replication and accumulation of disease-associated forms of the prion protein in MG20 cells up to the 15th passage. Furthermore, MG20 cells were susceptible to ME7, Obihiro scrapie, and bovine spongiform encephalopathy agents. Thus, MG20 cell lines persistently infected with various murine prion strains provide a useful model for the study of the pathogenesis of prion diseases.

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supporting

confidence: 58%

Microglial Cell Line Established from Prion Protein-Overexpressing Mice Is Susceptible to Various Murine Prion Strains

Iwamaru

Takenouchi

Ogihara

et al. 2007

J Virol

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“…The MG5 microglial cell line derived from p53-deficient mice was cultured in A1-cell conditioned medium (9). A1 cells were cultured in DMEM supplemented with 10% fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

Engulfment of Axon Debris by Microglia Requires p38 MAPK Activity

Tanaka¹,

Ueno

Yamashita

2009

Journal of Biological Chemistry

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The clearance of debris after injuries to the nervous system is a critical step for restoration of the injured neural network. Microglia are thought to be involved in elimination of degenerating neurons and axons in the central nervous system (CNS), presumably restoring a favorable environment after CNS injuries. However, the mechanism underlying debris clearance remains elusive. Here, we establish an in vitro assay system to estimate phagocytosis of axon debris. We employed a Wallerian degeneration model by cutting axons of the cortical explants. The cortical explants were co-cultured with primary microglia or the MG5 microglial cell line. The cortical neurites were then transected. MG5 cells efficiently phagocytosed the debris, whereas primary microglia showed phagocytic activity only when they were activated by lipopolysaccharide or interferon-␤. When MG5 cells or primary microglia were co-cultured with degenerated axons, p38 mitogen-activated protein kinase (MAPK) was activated in these cells. Engulfment of axon debris was blocked by the p38 MAPK inhibitor SB203580, indicating that p38 MAPK is required for phagocytic activity. Receptors that recognize dying cells appeared not to be involved in the process of phagocytosis of the axon debris. In addition, the axons undergoing Wallerian degeneration did not release lactate dehydrogenase, suggesting that degeneration of the severed axons and apoptosis may represent two distinct self-destruction programs. We observed regrowth of the severed neurites after axon debris was removed. This finding suggests that axon debris, in addition to myelin debris, is an inhibitory factor for axon regeneration.

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“…Mouse microglial cell line MG5 and mouse glial cell line A1 were maintained as previously described [35]. Mouse neuroblastoma cell line N1E-115 and Neuro 2a (American Type Culture Collection, Manassas, VA, USA) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 20 U/ml penicillin (Invitrogen, Gaithersburg, MD, USA), and 20 g/ml streptomycin (Invitrogen).…”

Section: Cell Culturementioning

confidence: 99%

Cooperative Therapeutic Action of Retinoic Acid Receptor and Retinoid X Receptor Agonists in a Mouse Model of Alzheimer's Disease

Kawahara

Suenobu

Ohtsuka

et al. 2014

JAD

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Abstract. Alzheimer's disease (AD) is a neurodegenerative process involving amyloid-␤ (A␤) peptide deposition, neuroinflammation, and progressive memory loss. Here, we evaluated whether oral administration of retinoic acid receptor (RAR)␣,␤ agonist Am80 (tamibarotene) or specific retinoid X receptor (RXR) pan agonist HX630 or their combination could improve deficits in an AD model, 8.5-month-old amyloid-␤ protein precursor 23 (A␤PP23) mice. Co-administration of Am80 (0.5 mg/kg) and HX630 (5 mg/kg) for 17 days significantly improved memory deficits (Morris water maze) in A␤PP23 mice, whereas administration of either agent alone produced no effect. Only co-administration significantly reduced the level of insoluble A␤ peptide in the brain. These results thus indicate that effective memory improvement via reduction of insoluble A␤ peptide in 8.5-month-old A␤PP23 mice requires co-activation of RAR␣,␤ and RXRs. RAR␣-positive microglia accumulated A␤ plaques in the A␤PP23 mice. Rat primary microglia co-treated with Am80/HX630 showed increased degradation activity towards 125 I-labeled oligomeric A␤ 1-42 peptide in an insulin-degrading enzyme (IDE)-dependent manner. The co-administration increased mRNA for IDE and membrane-associated IDE protein in vivo, suggesting that IDE contributes to A␤ clearance in Am80/HX630-treated A␤PP23 mice. Am80/HX630 also increased IL-4R␣ expression in microglial MG5 cells. The improvement in memory of Am80/HX630-treated A␤PP23 mice was correlated with the levels and signaling of hippocampal interleukin-4 (IL-4). Therefore, Am80/HX630 may promote differentiation of IL-4-responsive M2-like microglia and increase their activity for clearance of oligomeric A␤ peptides by restoring impaired IL-4 signaling in A␤PP23 mice. Combination treatment with RAR and RXR agonists may be an effective approach for AD therapy.

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Generation and characterization of a microglial cell line, MG5, derived from a p53-deficient mouse

Cited by 76 publications

References 51 publications

Microglial Cell Line Established from Prion Protein-Overexpressing Mice Is Susceptible to Various Murine Prion Strains

Microglial Cell Line Established from Prion Protein-Overexpressing Mice Is Susceptible to Various Murine Prion Strains

Engulfment of Axon Debris by Microglia Requires p38 MAPK Activity

Cooperative Therapeutic Action of Retinoic Acid Receptor and Retinoid X Receptor Agonists in a Mouse Model of Alzheimer's Disease

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