2004 Fiscal Year Final Research Report Summary
Regenerative therapy for acute lung injury based on intercellular cross talk
| Project/Area Number |
14370489
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kobe University |
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Principal Investigator |
OBARA Hidefumi Kobe University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (80030998)
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| Co-Investigator(Kenkyū-buntansha) |
MIKAWA Katsuya Kobe University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 助教授 (40229662)
NISHINA Kahoru Kobe University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (20311780)
MORIKAWA Osamu Kobe University, University Hospital, Instructor, 医学部附属病院, 助手 (50335436)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Acute lung injury / Apoptosis / Alveolar epithelial cells / Phosphodiesterase inhibitors / Bleomycin / Endotoxin / Endothelial progenitor cells / Neutrophils |
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| Research Abstract |
Regenerative therapy for acute lung injury consists of proliferation and repairment of alveolar epithelial and epithelial cells, and [3] prevention of lung fibrosis.CD34-positive cells were isolated from peripheral blood, and were differentiated to epithelial progenitor cells using EBM-2 medium containing VEGF, FBS, and IGF. In bleomycin-induced lung injury but not endotoxin-induced lung damage, blood microvessels were proliferated. The effects of rolipram (PDE-IV inhibitor) on proliferation of alveolar type II pneumocytes (AEC-II). Rolipram increased spontaneous proliperation and enhanced KGF/HGF-induced proliferation. Immunohistochemical analysis using BrdU antibody revealed that rolipram increased DNA synthesis in type II pneumocytes in mice treated with KGF/HGE. Acute lung injury was induced by intraperitoneal endotoxin in mice. Rolipram attenuated the morphological damages of the lung injury. We also biochemically and pathologically investigated whether exogenous intratracheal instillation of AEC-II isolated from rats can prevent fibrotic changes in endotoxin-induced lung injury. Intratracheal administration of AEC-II cells attenuated damage of epithelial cells and alveolar fibrosis although not significantly.
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Research Products
(11 results)
