期刊文献+

The expression of matrix metalloproteinases-9, transforming growth factor-β1 and transforming growth factor-β receptorⅠ in human atherosclerotic plaque and their relationship with plaque stability 被引量:23

The expression of matrix metalloproteinases-9, transforming growth factor-β1 and transforming growth factor-β receptorⅠ in human atherosclerotic plaque and their relationship with plaque stability
原文传递
导出
摘要 Background Transforming growth factor beta (TGF β) and matrix metalloproteinases 9 (MMP 9) have been implicated in the pathogenesis of human atherosclerosis but their relationship during lesion progression are poorly understood The objective of this study was to investigate the expression of MMP 9, TGF β1 and TGF β receptor Ⅰ (TβR Ⅰ) in human atherosclerotic plaque and their relationship and plaque stability Methods Specimens of human coronary artery atherosclerotic plaques were obtained from 41 patients undergoing coronary endarterectomy, and were paraffin embedded, sectioned at 4 μm intervals then stained with haematoxylin and eosin They were divided into stable (with no or only little lipid core) and unstable plaque groups (with lipid core size>40%): the immunohistochemical staining were performed for MMP 9,TGF β1 and TβR Ⅰ Results The expression of MMP 9 in the unstable plaques was much higher than in the stable ones, but the expression of TGF β1 was higher in the stable plaques There was no similar significant difference for TβR Ⅰ Correlation analysis showed that there was a negative correlation between the expression of MMP 9 and TGF β1 ( r =-0 332, P =0 034 for average areal density; r =-0 373, P = 0 016 for average optical density) Conclusions There were close relationships between MMP 9, TGF β1 and plaque stability Enhanced production of MMP 9 may participate in the formation of unstable plaque, while TGF β1 maybe an important stabilizing factor in preventing transition into an unstable plaque phenotype Background Transforming growth factor beta (TGF β) and matrix metalloproteinases 9 (MMP 9) have been implicated in the pathogenesis of human atherosclerosis but their relationship during lesion progression are poorly understood The objective of this study was to investigate the expression of MMP 9, TGF β1 and TGF β receptor Ⅰ (TβR Ⅰ) in human atherosclerotic plaque and their relationship and plaque stability Methods Specimens of human coronary artery atherosclerotic plaques were obtained from 41 patients undergoing coronary endarterectomy, and were paraffin embedded, sectioned at 4 μm intervals then stained with haematoxylin and eosin They were divided into stable (with no or only little lipid core) and unstable plaque groups (with lipid core size>40%): the immunohistochemical staining were performed for MMP 9,TGF β1 and TβR Ⅰ Results The expression of MMP 9 in the unstable plaques was much higher than in the stable ones, but the expression of TGF β1 was higher in the stable plaques There was no similar significant difference for TβR Ⅰ Correlation analysis showed that there was a negative correlation between the expression of MMP 9 and TGF β1 ( r =-0 332, P =0 034 for average areal density; r =-0 373, P = 0 016 for average optical density) Conclusions There were close relationships between MMP 9, TGF β1 and plaque stability Enhanced production of MMP 9 may participate in the formation of unstable plaque, while TGF β1 maybe an important stabilizing factor in preventing transition into an unstable plaque phenotype
出处 《Chinese Medical Journal》 SCIE CAS CSCD 2004年第12期1825-1829,共5页 中华医学杂志(英文版)
基金 ShenzhenScienceandTechnologyBureau(No200004052)
关键词 atherosclerotic plaque · matrix metalloproteinases 9 · transforming growth factor beta1 atherosclerotic plaque · matrix metalloproteinases 9 · transforming growth factor beta1
  • 相关文献

参考文献10

  • 1ChenS,ZhouZB,GuoY ,etal.Serummatrixmetalloproteinase9:apotentialclinicalmarkerforprognosisofcerebralinfarctionCerebrovasc[].DisForeignMedSci.2004
  • 2LutgensE,CleutjensKB,HeenemanS ,etal.BothearlyanddelayedantiCD40Lantibodytreatmentinduceastableplaquephenotype[].Proceedings of the National Academy of Sciences of the United States of America.2000
  • 3ChenSY,RobertJ.Transforming growthfactor:induceddifferentiationofsmoothmusclefromaneuralcreststemcellline[].Circulation Research.2004
  • 4HanssonGK,RobertsonAKL,GraingerDJ.TGF βinatherosclerosis[].ArteriosclerThrombVasc.2004
  • 5WeiLX,ShiHY,GuoAT ,etal.Morphologicdiscrepanciesofcoronaryatheroscleroticlesionsbetweenpatientswithstableandunstableanginaplusacutemyocardialinfarction[].ChinJPathol.1998
  • 6HongBK,KwonHM,LeeBK ,etal.Coexpressionofcyclooxygenase2andmatrixmetalloproteinasesinhumanaorticatheroscleroticlesions[].Yonsei Medical Journal.2000
  • 7MortenAK,PernilleH,KimH ,etal.Transforminggrowthfactorβcontrolshumanosteoclastogenesisthroughthep38MAPKandregulationofRANKexpression[].Journal of Biochemistry.2003
  • 8MallatZ,GojovaA,MarchiolFournigaultC ,etal.Inhibitionoftransforming growthfactorβsignalingacceleratesatherosclerosisandinducesanunstable plaque phenotypeinmice[].Circulation Research.2001
  • 9FeinbergMW,WatanabeM,LebedevaMA ,etal.Transforming growthfactor{beta}1inhibitionofvascularsmoothmusclecellactivationismediatedviasmad3[].Journal of Biochemistry.2004
  • 10LutgensE,GijbelM,SmookM ,etal.Transforminggrowthfactor betamediatesbalancebetweeninflammationandfibrosisduringplaqueprogression[].Arteriosclerosis Thrombosis and Vascular Biology.2002

同被引文献104

引证文献23

二级引证文献208

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部