1991 Fiscal Year Final Research Report Summary
Mechanism of glia maturation factor-induced differentiation of rat gioblasts
| Project/Area Number |
02670362
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Nagoya City University Medical School |
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Principal Investigator |
ITO Jin-ichi Nagoya City University Medical School, Assistant Professor, 医学部, 講師 (60167260)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Taiji Nagoya City University Medical School, Professor, 医学部・分子医学研究所, 教授 (60094364)
TANAKA Ryo Nagoya City University Medical School, Professor, 医学部, 教授 (90094383)
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| Project Period (FY) |
1990 – 1991
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| Keywords | glia maturation factor / rat glioblast / cell differentiation / 細胞骨格 |
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| Research Abstract |
Glia maturation factor(GNF), an acidic protein of H. W. 19.5 K, promotes both DNA synthesis and proliferation and induces morphological differentiation of rat glioblasts. Rat glioblasts treated with GMF gradually change to the mature astrocytic morphologies with the contracting cell bodies and the extending glial processes during 24 h to 48 h after GNF stimulation. Noticing the differentiation-inducing activity of GMF, We investigated the GMF activites to reorganize cytoskeletones of glioblasts by indirect immunofluorescence staining technique using anti-GFA protein antibody, anti-tubulinantibody, and NBDphallacidin in this study.
The microfilaments existing as the stress fibers before GNF treatment were reorganized to the plassaleanal undercort structure corelating to the morphological differentiation. The net work structures-forming microtubules and glia filaments in control cells were reformed to the thick filament structures by bundling foreation after GMF stimulation. Our experimental findings suggested that these alterations of cytoskeletal structures were regulated by the intracellular Ca^<2+> and caloodulin. After GMF stimulation, in rat astrocytes Ca^<2+> influx which had been increased prior to DNA synthesis was suppressed, and the caloodulin function also was inhibited following to cell division. The GHF-induced morphological differentiation was suppressed by the Ca ionophore-promoting rise of intracellular Ca^<2+> level and promoted with W 7, a calsodulin antagonist, suggesting the dependency on the suppression of caloodulin activity.
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