2003 Fiscal Year Final Research Report Summary
Regenerative medicine for acute lung injury : introduction of EPC
| Project/Area Number |
13671579
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 |
MIKAWA Katsuya Kobe University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (40229662)
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| Co-Investigator(Kenkyū-buntansha) |
NISHINA Kahoru Kobe University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (20311780)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Acute lung injury / Apoptosis / Bleomycin / Alveolar epithelial cells / Phosphodiesterase inhibitors / Endotoxin / Neutrophils / 好中球 |
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| Research Abstract |
CD34-positive cells were isolated from peripheral blood. These cells were differentiated to epithelial progenitor cells (EPC) using EBM-2 medium containing VEGF, FBS, and IGF. Using ARDS experimental model, dynamic change of endothelial cells was immunohistologically assessed by surface antigen. In bleomycin-induced acute lung injury, proliferation of blood vessels was observed. However, vascular proliferation did not occur in endotoxin-induced lung injury. We investigated the effects of rolipram (PDE-IV inhibitor), lidocaine, midazolam, propofol, ketamine (anesthetics) on proliferation of alveolar type II pneumocytes. Rolipram increased spontaneous proliperation and enhanced KGF/HGF-induced proliferation of rat cultured type II pneumocytes. Lidocaine, midazolam, propofol, ketamine had no effect on spontaneous proliperation and enhanced KGF/HGF-induced proliferation of type II pneumocytes. Anti-Fas antibody-induced apoptosis of neutrophils was enhanced by rolipram and not by the anesthetics. Immunohistochemical analysis using BrdU antibody revealed that rolipram increased DNA synthesis in type II pneumocytes in mice treated with KGF/HGF. Rolipram attenuated the pathological changes of the endotoxin-induced acute lung injury. This successful result of rolipram may be due to the effect of the drug on alveolar epithelial cells.
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