Tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion.

Q Z Feng, T D Li, L X Wei, X Qiao, J Yi, L Wang, T S Yang
{"title":"Tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion.","authors":"Q Z Feng,&nbsp;T D Li,&nbsp;L X Wei,&nbsp;X Qiao,&nbsp;J Yi,&nbsp;L Wang,&nbsp;T S Yang","doi":"10.1136/mp.56.6.362","DOIUrl":null,"url":null,"abstract":"<p><strong>Aims: </strong>To explore the role of Fas in cardiomyocytic apoptosis induced by ischaemia through determining the histological relation between Fas expression and apoptosis in rat myocardium during ischaemia/infarction.</p><p><strong>Methods: </strong>The myocardial ischaemia model was produced by ligating the left coronary artery in Sprague-Dawley rats. The rats were killed from 10 minutes to seven days after surgery. Apoptotic myocardial cells were detected by the in situ terminal deoxynucleotidyl transferase mediated nick end labelling method, and the expression of Fas by immunohistochemistry and western blotting.</p><p><strong>Results: </strong>Cardiomyocytic apoptosis appeared from three to 36 hours after ischaemia. The expression of Fas could be detected by western blot from before surgery to seven days of ischaemia. Apoptosis and the expression of Fas in the cardiomyocytes appeared in different regions of the myocardium: apoptosis in the ischaemic region, Fas in the regions surrounding ischaemic myocardium.</p><p><strong>Conclusion: </strong>These results suggest that there is a tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion. Fas might not directly regulate the apoptosis of cardiomyocytes induced by ischaemia.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 6","pages":"362-7"},"PeriodicalIF":0.0000,"publicationDate":"2003-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.6.362","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular pathology : MP","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1136/mp.56.6.362","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 8

Abstract

Aims: To explore the role of Fas in cardiomyocytic apoptosis induced by ischaemia through determining the histological relation between Fas expression and apoptosis in rat myocardium during ischaemia/infarction.

Methods: The myocardial ischaemia model was produced by ligating the left coronary artery in Sprague-Dawley rats. The rats were killed from 10 minutes to seven days after surgery. Apoptotic myocardial cells were detected by the in situ terminal deoxynucleotidyl transferase mediated nick end labelling method, and the expression of Fas by immunohistochemistry and western blotting.

Results: Cardiomyocytic apoptosis appeared from three to 36 hours after ischaemia. The expression of Fas could be detected by western blot from before surgery to seven days of ischaemia. Apoptosis and the expression of Fas in the cardiomyocytes appeared in different regions of the myocardium: apoptosis in the ischaemic region, Fas in the regions surrounding ischaemic myocardium.

Conclusion: These results suggest that there is a tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion. Fas might not directly regulate the apoptosis of cardiomyocytes induced by ischaemia.

冠脉闭塞后Fas表达与细胞凋亡的时空分离。
目的:通过测定大鼠缺血/梗死心肌中Fas表达与细胞凋亡的组织学关系,探讨Fas在缺血心肌细胞凋亡中的作用。方法:结扎左冠状动脉造心肌缺血模型。这些老鼠在手术后10分钟到7天内被杀死。采用原位末端脱氧核苷酸转移酶介导的缺口末端标记法检测心肌细胞凋亡,免疫组织化学和免疫印迹法检测Fas表达。结果:缺血后3 ~ 36 h出现心肌细胞凋亡。从术前到缺血7 d, western blot均可检测Fas的表达。心肌细胞凋亡和Fas的表达出现在心肌的不同区域:缺血区凋亡,缺血心肌周围区Fas。结论:冠状动脉闭塞后Fas的表达与细胞凋亡存在时空分离关系。Fas可能不直接调控缺血引起的心肌细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信