2007 Fiscal Year Final Research Report Summary
Role of fibrocytes, a newly identified tone marrow-derived cells, in the pathogenesis of renal fibrosis
| Project/Area Number |
18590887
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
WADA Takashi Kanazawa University, Graduath Schcol of Medical Science, Professor (40334784)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Keywords | fibre cote / chemokine / kidney / fibrosis / renin / angiotensin / angiotensin recentor / collagen |
|---|
| Research Abstract |
Fibrocytes are supposed to be a circulating connective tissue cell progenitor that consists of a novel population of peripheral blood cells. This distinct population of blood-borne cells shares markers of leukocytes as well as mesenchymal cells. Accumulating evidence indicates that fibrosis is characteristic of progressive chronic kidney diseases of any etiologies, resulting in kidney failure. We have uncovered that CCR7-positive fibrocytes migrate into the kidney in response to secondary lymphoid tissue chemokine (SLC/CCL21) and contribute to kidney fibrosis induced by unilateral ureteral obstruction in mice. In addition, the blockade of CCL21/CCR7 signaling by anti-CCL21 antibodies reduced kidney fibrosis, which was confirmed by a decrease in fibrosis in CCR7-null mice with concomitant reduction in macrophage recruitment along with reduced renal transcripts of monocyte chemoattractant protein-1 (MCP-1/CCL2). In addition, angiotensin receptor type 1 /type 2 signaling may contribute to the pathogenesis of renal fibrosis by at least two mechanisms: (1) by regulating the number of fibrocytes in bone marrow, and (2) by direct activation of fibrocytes via these two receptors. These findings suggest that fibrocytes dependent on CCL21/CCR7 signaling pathways and renin-angiotensin system contribute to the pathogenesis of kidney fibrosis, thereby providing that regulating fibrocytes may provide a novel therapeutic benefit for kidney fibrosis.
|
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
[Presentation] 慢性腎臓病とケモカイン2007
Author(s)
和田隆志, 他
Organizer
第28回日本炎症・再生医学会シンポジウム
Place of Presentation
東京
Year and Date
2007-08-03
Description
「研究成果報告書概要(和文)」より
-
-
-
-
-
-
-
-
