| Project/Area Number |
03670317
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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 |
内科学一般
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SASAKI Sei Tokyo Medical and Dental University, Assistant Professor, 医学部, 講師 (60170677)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAMOTO Hisato same as above, Instructor, 医学部, 助手 (80187046)
ISHIBASHI Kenichi same as above, Instructor, 医学部, 助手 (80223022)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1991: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | ET / HGF / Mesangial cells / Nephritis / Acute Renal Failure / 腎炎 / 急性腎不全 |
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| Research Abstract |
(1) Endothelin (ET): We showed that growth factors stimulated ET-1 production via protein kinase C pathways in mesangial cells. On the other hand, b-agonist inhibited the production by protein Kinase A mediated mechanisms (Kidney Int 41:350, 1992). By using RT-PCR and Northern methods we observed that ET receptors types changed during cell cycle in cultured mesangial cells. A new vasoactive substance, nitric oxide (NO) stimulated the ET-1 production. Now study is in progress in experimental and human nephritis.
(2) Hepatocyte Growth Factor (HGF): We showed that HGF mRNA expressed in mesangial cells, but not in renal epithelial cells. mRNA of c-met (HGF receptor)was expressed in epithelial cells, but not in mesangial cells. HGF showed mitogenic action and stimulated NaK-ATPase in epithelial cells, and no effects in mesangial cells (BBRC 182:960, 1992). Thus, HGF is a paracrine factor for renal epithelial cells. Both HGF and c-met mRNA expression was enhanced in uninephrectomy, ishemic injury (BBRC 187:1454, 1992). These data taken together, HGF may function as an important modulator and renotropic factor in normal diseased states.
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