| Project/Area Number |
61570862
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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 |
Morphological basic dentistry
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| Research Institution | Iwate Medical University |
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Principal Investigator |
HATAKEYAMA Setsuko School of Dentistry, associate assistant, 歯学部, 助手 (70048495)
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| Co-Investigator(Kenkyū-buntansha) |
SASHIMA Mieko School of Dentistry, associate assistant, 歯学部, 助手 (40048575)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Glucocorticoid / Glucocorticoid receptor / Salivary gland tumor / Cell growth / Cellular differentiation / Cell cycle / Flow cytometry / Nude mouse / ヌードマウス / 細胞増殖 / 株細胞 / 細胞肥大ヌードマウス |
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| Research Abstract |
1) Glucocorticoids induced the inhibition of cellular proliferation (the dectease of DNA synthesis, the prolongation of doubling time, and the decrease of the rate of colony formation) and morphological change of HSG cells after the treatment for 8-16 hours at concentrations of 0.01-0.1 muM. Scatchard plot analysis using [6,7-^3H]-triamcinolone revealed that the HSG cells had apparent cytosolic glucocorticoid receptors with an equilibrium dissociation constant (Kd value) of 6.5 nM whose number of binding sites was 57.8 fmol/mg protein. 2) Glucocorticoids also showed growth-inhibitory effects such as a suppression of tumor growth, the appearance of duct-like structures, and epithelial membrane antigen (EMA)-immunoreactive cells by histological observation of HSG cells transplanted in nude mice by mediating the specific receptors. 3) Glucocorticoids arrested G0-G1 phase in the cell cycle of HSG cells by blocking the transition of G0-G1 to S phase. The action of G0-G1 arrest was observed only in the medium with serum or supplements (10mug/ml insulin, 10 mug/ml transferrin, and 20 mug/ml monoethanolamine) and was nullified by additive EGF (10 ng/ml). Conditioned medium and supplements (insulin, transferrin, and monoethanolamine) did not suppress G0-G1 arrest-effect of glucocorticoids. The simultaneous additions of glucocorticoid and cycloheximide (which was the blocker of protein synthesis) suppressed the glucocorticoid-induced G0-G1 arrest. These results indicate that glucocorticoids probably induce some growthinhibitory factors for HSG cells which compete with the growthstimulating effect of EGF.
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