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KMID : 0368120020320100884
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Korean Circulation Journal
2002 Volume.32 No. 10 p.884 ~ p.893
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Expression of Nitric Oxide Synthase Isoforms after Endothelial Denudation of the Rat Carotid Artery
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김동운/Dong Woon Kim
권진숙/이광주/김기석/최소영/박해남/기주영/연태진/김영규/조명찬/Jin Sook Kwon/Kwang Ju Lee/Ki Seok Kim/So Young Choi/Hai Nan Piao/Joo Young Ki/Tae Jin Youn/Young Gyu Kim/Myeong Chan Cho
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Abstract
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b>Background and Objectives: The nitric oxide synthase (NOS) system may be involved in the healing process following arterial injury. The expressions of eNOS or iNOS have been observed separately following endothelial denudation of rat carotid arteries. However, the expressions of nitric oxide synthase isoforms (eNOS, iNOS and nNOS) have not been observed simultaneously.
Materials and Methods: Using balloon catheter denudation of the rat carotid artery, as a model for arterial injury and restenosis, we have evaluated the time course of the expressions of eNOS, iNOS and nNOS simultaneously using immunohistochemistry and RT-PCR.
Results: From the immunohistochemistry, the iNOS protein was shown to be rapidly induced following injury (day 1) and was later seen to be relocalized to the neointima (day 5). Two weeks following injury the iNOS expression had declined. After 4 weeks the iNOS expression had disappeared completely. The eNOS protein was not detected until three days post injury. Two weeks following injury the eNOS expression was observed at the “pseudoendothelial” surface forming intimal smooth muscle cells. By week 4 the eNOS expression was detected on the morphological endothelium. The nNOS expression was detected at the media one day following injury and for the subsequent two weeks, but it was not detected at the neointima at all. RT-PCR demonstrated
that iNOS mRNA was faintly expressed 1 day following endothelial denudation. The expression level of the iNOS mRNA was highest at 5 days, but gradually decreased until 2 weeks following injury.
Conclusion: These results suggest that endothelial disruption may induce the expressions of iNOS and nNOS, and the re-expression of eNOS may reduce these expressions. The expressions of iNOS and nNOS could be a homeostatic mechanism that compensates for the loss of endothelium.
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KEYWORD
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Nitric-oxide synthase, Angioplasty, Restenosis,
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