2006 Fiscal Year Final Research Report Summary
A treatment strategy of inflammatory bowel disease using endothelial progenitor cell
Project/Area Number |
16590647
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
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Research Institution | Kurume University |
Principal Investigator |
MITSUYAMA Keiichi Kurume University School of Medicine, Department of Medicine, Associate professor, 医学部, 助教授 (20200066)
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Co-Investigator(Kenkyū-buntansha) |
TOMIYASU Nobuo Kurume University School of Medicine, Department of Medicine, Assistant, 医学部, 助手 (20289424)
SUZUKI Asuka Kurume University School of Medicine, Department of Medicine, Assistant, 医学部, 助手 (30341324)
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Project Period (FY) |
2004 – 2006
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Keywords | Inflammatory bowel disease / Endothelial progenitor cell / Regenerative therapy / Ulcerative colitis / Crohn's disease / Neovascularization |
Research Abstract |
At first we differentiated endothelial progenitor cells (EPC) from peripheral blood mononuclear cells and confirmd these cells as EPC using a stem cell marker CD 34 as well as vascular endothelial cell markers Lectin, Flk-1, VE-cadherin and acLDL. Next, we examined the number of EPC and hematopoietic stem cells of patients with inflammatory bowel disease (IBD) and infectious colitis and healthy subjects. It should be noted that the number of EPC was decreased in active ulcerative colitis (UC) patients compared to Crohn's disease-and infectious colitis patients and healthy subjects. EPC was increased in infectious colitis patients compared to healthy subjects. In UC patients the number of EPC correlated positively with serum hemoglobin levels and negatively with the platelet number. Furthermore we measured the number of BFU-E, CFU-G, CFU-GM, CFU-GEMM and CFU-F colonies. However, each of these colonies did not show significant differences among any groups. These data indicated that the decrease of EPC seen in UC may be caused by the impairment of EPC differentiation. In the next step, we examined the effect of exogenous EPC on the severity of DSS-induced colitis. On the 3^<rd> day following the initial DSS drinking mice received EPC (1×10^6 cells/animal) or PBS intravenously from the tail vein. We observed significant improvement of the weight loss in the EPC group compared with the PBS group. We also found the tendency of improvement in clinical scores and the colon length in the EPC group. Taken together, the administration of EPC may betherapeutic for IBD. At present we are carrying out the additional experiments to confirm these results.
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Research Products
(1 results)