2003 Fiscal Year Final Research Report Summary
HISTOLOGICAL EXMINATION OF CELL CYCLE REGULATOR EXPRESSION AFTER CORONARY STENTING
| Project/Area Number |
14570696
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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 |
Circulatory organs internal medicine
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| Research Institution | SHOWA UNIVERSITY |
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Principal Investigator |
SAKAI Tetsuo SHOWA UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (60281367)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Tsukasa SHOWA UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (40205662)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Coronary stent / Restenosis / Neointima / Vascular smooth muscle cell / Cell cycle regulator / Cdk inhibitor / Histopathlogy / Immunohistochemistory |
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| Research Abstract |
Background Proliferation of vascular smooth muscle cells (VSMCs) is under the control of cell cycle regulator activity, which is induced by several growth factors. Recent attention has been drawn to treatments that target cell cycle regulators to prevent the proliferation of VSMCs after coronary angioplasty. However, histopathological evaluation of cell cycle regulator expression after human coronary stenting has not been sufficient.
Methods and Results Thirty-six coronary arteries of 27 cadavers were examined. Time from stent implantation to patient death ranged from 0 to 235 days. Sections were stained with antibodies against platelet-derived growth factor (PDGF), basic fibroblast growth factor (b-FGF), cyclin D1, p16, p21, and p27. To detect redifferentiated VSMCs, staining for macrophage colony stimulating factor receptor (MCSF-R) was done.
MCSF-R-positive cells were observed in neointima but decreased in the late stage. PDGF was detected in neointima and decreased gradually. Expression of cyclin D1 appeared to be associated with the proliferation of VSMCs, whereas p27 was downregulated with the proliferation of neointima and upregulated in the late stage.
Conclusions Our results suggest that one of the most promising methods for preventing excessive proliferation of neointima after stenting is to limit the decrease of p27 or the increase of cyclin D1.
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