| Project/Area Number |
08671287
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Okayama University |
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Principal Investigator |
MAKINO Hirofumi (1997) Okayama University Medical School, Professor, 医学部, 教授 (50165685)
四方 賢一 (1996) 岡山大学, 医学部, 助手 (00243452)
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| Co-Investigator(Kenkyū-buntansha) |
KUNITOMI Mie Okayama University Medical School Hospital, Senior Resident, 医学部・附属病院, 医員
TSUCHIYAMA Yoshinori Okayama University Medical School Hospital, Senior Resident, 医学部・附属病院, 医員
SHIKATA Kenichi Okayama University Medical School Hospital, Lecturer, 医学部・附属病院, 講師 (00243452)
山地 浩明 岡山大学, 医学部・附属病院, 医員
林 佳子 岡山大学, 医学部・附属病院, 医員
槙野 博史 岡山大学, 医学部, 教授 (50165685)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Kidney / Adhesion molecule / ICAM-1 / Selectin / Glomerulonephritis / Diabetes / Sulfatide / Therapy / 炎症 / 免疫 / マクロファージ / 好中球 |
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| Research Abstract |
We have investigated the possibility of application of anti-cell adhesion molecule therapies for renal diseases. In summary,
1. We showed the up-regulated expression of ICAM-1, E-selectin and P-selectin in the glomeruli and interstitium of the kidney or the patients with glomerulonephritis and diabetic nephropathy.
2. We calrified the mechanism that glomerular hyperfiltration induces intraglomerular expression of ICAM-1 and infiltration of macrophages.
3. We showed that the ligands for L-selectin exist in the cytoplasm of tubular epithelial cells and re-distribute to the interstitium and peritubular capillaries after ureteral ligation in rat kidney. Furthermore, we showed that one of the ligands for L-selectin is sulfatide.
4. We showed that administration of sulfatide which is a ligand for L- and P-selectin inhibits the infiltration of macrophage to renal interstitium in vivo.
5. We showed that prostaglandin I_2 ameliorates renal injury by inhibition of ICAM-1 expression in rat crescentic glomerulonephritis model.
These results showed the critical role of ICAM-1 and selectins for the infiltration of macrophege into renal tissues in various types of glomerular diseases. In conclusion, our results suggest the beneficial effects of anti-cell adhesion molecule therapy for glomerular diseases.
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