| Project/Area Number |
09671169
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | KUMAMOTO UNIVERSITY |
|---|
Principal Investigator |
KITAMOTO Yasunori Kumamoto University School of Medicine, 3rd Department of Internal Medicine, Associate Professor, 医学部, 講師 (80195297)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TOMITA Kimio Kumamoto University School of Medicine, 3rd Department of Internal Medicine, Pro, 医学部, 教授 (40114772)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
|---|
| Keywords | endogenous VEGF / adult kidney / neutralizing antibody / endothelial degeneration / 維持修後 / Thy-1腎炎 / 糸球体リモデリング / 腎の発生 / 糸球体血管内皮細胞 |
|---|
| Research Abstract |
The glomerulus in the kidney is fenestrated and coiled capillary structure with afferent and efferent arterioles and its endothelial cells are exposed to much higher pressure and shear stress than in any other capillaries. Vascular endothelial growth factor (VEGF) mediates blood vessel formation in response to developmental, tumor, inflammatory or endocrine signals, but a role in the maintenance of normal developed vessels has not been demonstrated. Here we show that suppression of endogenous VEGF activity by antibody caused the degeneration of endothelial cells and the obstruction of capillaries in the renal glomeruli in mice. VEGF production in the human kidney may be compensatively elevated as a response to the irreversible loss of glomeruli in glomerulonephritis. In experimental glomerulonephritis, exogenous VEGF prevented the rupture of glomerular capillaries. These results indicate that VEGF supports endothelial cells to maintain the glomerular architecture under physiological and pathological stresses.
|
