2003 Fiscal Year Final Research Report Summary
Molecular mechanism of spontaneous remission from renal injury
| Project/Area Number |
13671118
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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 | Nagasaki University |
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Principal Investigator |
MIYAZAKI Masanobu Nagasaki University, Hospital Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (10246100)
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| Co-Investigator(Kenkyū-buntansha) |
KONHO Shigeru Nagasaki University, Postgraduate School of Medicine, Professor, 大学院・医歯薬学総合研究科, 教授 (80136647)
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| Project Period (FY) |
2001 – 2003
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| Keywords | angiotensin II / aldosterone / angiogenesis / glomerulonephritis / VEGF / CYP11B2 |
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| Research Abstract |
In the present study, we examined the role of angiotensin II in the process of spontaneous remission of glomerular injury in experimental mesangial proliferative glomerulonephritis and tested the expression of mRNA for CYP11B, the key enzyme of aldosterone synthesis in human renal biopsy specimens using in situ hybridization. We induced reversal mesangial proliferative glomerulonephritis by Habu-snake venom injection. Compared with wild type mice, the delay of remission from glomerular injury, including expansion of mesangial area and reduced number of glomerular capillary wall, was observed in mice without angiotensin II receptor type 1. Treatment of VEGF (vascular endothelial cell growth factor) promoted restoration of glomerularr injury in the model. In the second study, CYP11B2 mRNA was expressed in glomerular cells, such as mesangial cells, glomerular epithelial and endothelial cells, and infiltrating cells and atrophic tubular cells in the interstitium. Moreover, these expressions of CYP 11 B2 mRNA were significantly correlated with the degree of their tissue injury. Our results suggested that angiotensin II is important in the reconstitution of glomerular capillary and that aldosterone produced in human renal tissue was involved in renal tissue damage.
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