Increased immunoreactive endothelin-1 in human transplant coronary artery disease.
Increased immunoreactive endothelin-1 in human transplant coronary artery disease.
复制标题
人类移植冠状动脉疾病中免疫反应性内皮素-1 增加。
DOI:
10.1161/01.cir.94.9.2096
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发表时间:
1996
期刊:
影响因子:
37.8
通讯作者:
Cannon,PJ
中科院分区:
文献类型:
--
作者:
Ravalli,S;Szabolcs,M;Albala,A;Michler,RE;Cannon,PJ
BackgroundThe pathogenesis of transplant coronary artery disease (TCAD) is unknown, but it is thought to derive from an interaction between immune and nonimmune factors, leading to smooth muscle cell proliferation and accumulation in the expanded neointima. Endothelin-1 (ET-1), a potent vasoconstrictor with mitogenic properties for vascular smooth muscle cells, has recently been demonstrated in native vessel atherosclerosis. The present study used immunohistochemistry to investigate the role of ET-1 in TCAD.Methods and ResultsET-1 immunoreactivity and cellular localization were assessed in human coronary arteries with TCAD (n=13) and in normal coronary arteries (n=10) with single- and double-label immunohistochemistry. The intensity of immunostaining was determined by a semiquantitative method. Diffuse and intense ET-1 immunoreactivity was found in 11 of 13 patients with TCAD (85%), mainly in myointimal cells and, in lesser amounts, in macrophages and endothelial cells. In contrast, normal coronary arteries had only faint immunostaining localized to the endothelial layer. Mean semiquantitative grade was significantly higher in TCAD than in normal arteries (1.8 versus 0.7;P<.05). ET-1 was more frequently present in lipid-rich, atheromatous lesions than in lipid-poor, proliferative ones. Intimal neovessels consistently immunostained for ET-1.ConclusionsImmunoreactivity for ET-1 is significantly increased in TCAD, possibly as a result of stimulatory cytokines and growth factors that are upregulated in the posttransplant state. The results suggest a role for this mitogenic peptide in the pathogenesis of graft arteriosclerosis.
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影响因子:
6
作者:
M. Kowala;Patricia M. Rose;D. Philip;Stein;Nancy Goller;R. Recce;Sophie Beyer;M. Valentine;Debbie Barton;Stephen K. Durham
通讯作者:
Stephen K. Durham
影响因子:
15.9
作者:
Timothy;E.;Bunchman;Craig;A. Brookshire
通讯作者:
A. Brookshire
影响因子:
20.1
作者:
Stephen A. Douglas;C. Louden;L. Vickery;B. Storer;Timothy Hart;G. Feuerstein;John D. Elliott;E. Ohlstein
通讯作者:
E. Ohlstein
影响因子:
5.2
作者:
T. Masaki
通讯作者:
T. Masaki
DOI:
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发表时间:
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期刊:
影响因子:
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作者:
通讯作者:
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