2002 Fiscal Year Final Research Report Summary
Role of Midkine in Glomerular and Tubulointerstitial Injuries
| Project/Area Number |
13671111
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
YUZAWA Yukio Nagoya University, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 講師 (00191479)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KADOMATSU Kenji Nagoya University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (80204519)
MATSUO Seiichi Nagoya University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (70190410)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Keywords | Midkine / tubulointerstitial injury / glomerular injury / antisense ODN / knockout mouse / coagulatio-fibrynolysis / Th1 / Th2 |
|---|
| Research Abstract |
Midkine (MK) is a mutepotentioal heparin-binding growth factor with migration-promoting activity for neutrophils, macrophages and neurons. Although MK expression is mainly limited in the course of nephrogenesis, the enhanced expression of MK is also observed in the tubular epithelial cells in the diseased kidney. The role of MK in tubulointerstitial injuries as well as in glomerular injuries was studies. MK induces the chemotaxis of inflammatory leukocytes into the tubulointerstitium at least partially through the induction of MCP-I and MIP-2, and that MK contributes the aggravation of ischemia-induced tubulointerstitial damage.
MK anti-sense oligonucleotide (ODN) distributes in the proximal tubular epithelial cells, which is the main part for de novo MK expression, after intravenous injection, and significantly reduced the expression of MK in the tubules. Consequently, MK antisense ODN successfully block the ischemic reperfusion injuries in the tubulointerstitium.
These results strongly suggest that MK antisense ODN appears to be a candidate for the novel therapeutic approaches in ischemia-induced tubulointerstitial injuries.
|
-
-
-
-
-
-
-
-
-
[Publications] Ikeguchi H, Maruyama S, Morita Y, Fujita Y, Kato T, Natori Y, Akatsu H, Campbell W, Okada N, Okada H, Yuzawa Y, Matsuo S: "Effects of human soluble thrombomodulin on experimental glomer ulonephritis"Kidney International. 61. 490-501 (2002)
Description
「研究成果報告書概要(欧文)」より
-
