2001 Fiscal Year Final Research Report Summary
Molecular Mechanism of the role of oxidized LDL and physical stress in progressive renal disease
| Project/Area Number |
12671023
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
KANAME Shinya Facuity of Medicin Nephrology and Endocrmology, The University of Tokyo, The Dept of Assistant Professor, 医学部・附属病院, 助手 (60224581)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Keywords | oxidized LDL / Lox-1 / progressive renal disease |
|---|
| Research Abstract |
In this study, we investigated LOX-1 expression and its localization in 5/6 subtotal nephrectomized (5/6 Nx) rats. 6 weeks after 5/6 Nx, blood pressure, serum creatinine and serum cholesterol were significantly increased compared with sham operated rats. Northern blot showed that LOX-1 mRNA levels in the whole kidney were markedly elevated in 5/6 Nx rats compared with control rats. Immunohistochemical analysis using polyclonal anti-LOX-1 antibody showed that in 5/6 Nx rats some glomerular cells were weakly positive, but interestingly, strong staining was widely observed in the interstitial cells including macrophages and peritubular endothelial cells, although there is no staining in the tubules. LOX-1 is almostjiegative in the control rats. Moreover, preliminary results showed that the LOX-1 expression decreased, as well as blood pressure, by administrating ATI antagonist candesartan (10 mg/kg/day) in 5/6 Nx rats. These results indicate that LOX-1 is upregulated in the kidney of rat model for chronic renal diseases, especially in the interstitial cells, suggesting that the increased LOX-1 might play some roles in the progression of interstitial and glomerular injury.
|
Research Products
(2 results)
