| Project/Area Number |
06671160
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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 |
Kidney internal medicine
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| Research Institution | Tokyo Women's Medical College |
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Principal Investigator |
NIHEI Hiroshi Tokyo Women's Medical College, School of Medicine, Professor, 医学部, 教授 (30124308)
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| Co-Investigator(Kenkyū-buntansha) |
TSUCHIYA Ken Tokyo Women's Medical College, School of Medicine, Lectuler, 医学部, 助手 (00246472)
NITTA Kosaku Tokyo Women's Medical College, School of Medicine, Lectuler, 医学部, 助手 (50241071)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Fibroblast / TGF-beta / extracellular matrix / pertussis toxin / peptide / G-protein / G蛋白 / フィブロネクチン |
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| Research Abstract |
The aim of the project is to clarify if G-protein is involved in the regulation of TGF-beta-induced extracellular matrix. Normal rat kidney (NRK) cells were incuvated for 24 h in the presence or absence of various concentration of TGF-beta. TGF-beta increased fibronectin accumulation in the supernatant in a dose-dependent manner without stimulation of cell proliferation. Moreover, 100 nM pertussis toxin (PTX) did not inhibit this effect. Therefore, we speculated that TGF-beta-induced fibronectin accumulation might be linked to PTX-insensitive G-protein. We systhesized several tipes of peptides which were cytoplasmic domains of several types of Galpha-subunits, according to Nishimoto's motif (J.Biol.Chem.269 ; 13756,1994). 22 amino acids (NNIQVVEDAVTDIIIANNLRC) indicating cytoplasmic domain of Goalpha inhibited 500 pM of TGF-beta increased fibronectin accumulation with IC50 of 1 muM.These results suggest that PTX-insensitive Go is involved in the TGF-beta-induced fibronectin accumulation.
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