2006 Fiscal Year Final Research Report Summary
Restoration of renal microcirculation by eNOS gene transfection for overcoming the antibody-mediated rejection and achievement of long-term renal allograft survival
Project/Area Number |
15390487
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
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Research Institution | Niigata University |
Principal Investigator |
TAKAHASHI Kota Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (90101857)
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Co-Investigator(Kenkyū-buntansha) |
SAITO Kazuhide Niigata University, Medical and Dental Hospital, Lecturer, 医歯学総合病院, 講師 (20262438)
OITE Takashi Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (60018744)
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Project Period (FY) |
2003 – 2006
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Keywords | microcirculation injury / ischemia-reperfusion injury / renal vascular endothelial cells / rat bone marrow transplantation / GFP positive cells / stem cell transplantation |
Research Abstract |
1. From the clinicopathological observation of antibody-mediated rejection in living donor ABO-incompatible kidney transplantation and ischemia-reperfusion injury in deceased donor kidney transplantation, We had analyzed and evaluated the process of the microcirculation injury and microvascular endothelial cell damage. 2. We had established the GFP(+) to (-) rat bone marrow transplantation model and evaluated the role of The bone marrow derived endothelial progenitor cells in the regeneration of the injured microvascular Cells in renal ischemia-reperfusion injury. 3. We have revealed that the bone marrow derived endothelial cells have migrated and recovered the injured endothelial cells in renal ischemia-reperfusion injury. It was approved not only by static immunohinstopathological method but also by dynamic direct observation by real-time phase contrast microscopy. 4. We have also established in vitro eNOS gene transfection into cultured vascular endothelial cells, However, transplantation and restoration of injured endothelial cells by eNOS transfectant endothelial cells in "in vivo" experimental model could not be established. 5.These result will be useful for the clinical renal preservation and regeneration therapy for antibody-mediated rejection in ABO-incompatible kidney transplantation and ischemia-reperfusion injury in deceased donor kidney transplantation.
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Research Products
(12 results)