PSYCH OpenIR  > 脑与认知科学国家重点实验室
Reactive carbonyl compounds (RCCs) cause aggregation and dysfunction of fibrinogen
Xu, Ya-Jie1; Qiang, Min1,2; Zhang, Jin-Ling1; Liu, Ying1; He, Rong-Qiao1,3; He, RQ (reprint author), Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China.
心理所单位排序1,3
摘要Fibrinogen is a key protein involved in coagulation and its deposition on blood vessel walls plays an important role in the pathology of atherosclerosis. Although the causes of fibrinogen (fibrin) deposition have been studied in depth, little is known about the relationship between fibrinogen deposition and reactive carbonyl compounds (RCCs), compounds which are produced and released into the blood and react with plasma protein especially under conditions of oxidative stress and inflammation. Here, we investigated the effect of glycolaldehyde on the activity and deposition of fibrinogen compared with the common RCCs acrolein, methylglyoxal, glyoxal and malondialdehyde. At the same concentration (1 mmol/L), glycolaldehyde and acrolein had a stronger suppressive effect on fibrinogen activation than the other three RCCs. Fibrinogen aggregated when it was respectively incubated with glycolaldehyde and the other RCCs, as demonstrated by SDS-PAGE, electron microscopy and intrinsic fluorescence intensity measurements. Staining with Congo Red showed that glycolaldehyde-and acrolein-fibrinogen distinctly formed amyloid-like aggregations. Furthermore, the five RCCs, particularly glycolaldehyde and acrolein, delayed human plasma coagulation. Only glycolaldehyde showed a markedly suppressive effect on fibrinogenesis, none did the other four RCCs when their physiological blood concentrations were employyed, respectively. Taken together, it is glycolaldehyde that suppresses fibrinogenesis and induces protein aggregation most effectively, suggesting a putative pathological process for fibrinogen (fibrin) deposition in the blood.
关键词fibrinogen acrolein glycolaldehyde glyoxal malondialdehyde methylglyoxal
学科领域Physiological Psychology/biological Psychology
2012-08-01
语种英语
发表期刊PROTEIN & CELL
ISSN1674-800X
卷号3期号:8页码:627-640
期刊论文类型Article
URL查看原文
收录类别SCI
项目简介We thank Dr. Joy Fleming for helpful comments and improving the English of the manuscript. This work was supported by the National Basic Research Program (973 Program) (Grant Nos. 2010CB912303 and 2012CB911004), and the Natural Scientific Foundation of China (Grant Nos. NSFC 30970695 and QBI-IBP GJHZ1131).
WOS记录号WOS:000310531900009
资助机构National Basic Research Program (973 Program) [2010CB912303, 2012CB911004] ; Natural Scientific Foundation of China [NSFC 30970695, QBI-IBP GJHZ1131]
引用统计
被引频次:23[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/12909
专题脑与认知科学国家重点实验室
通讯作者He, RQ (reprint author), Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China.
作者单位1.Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China
2.Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China
3.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, Beijing 100101, Peoples R China
第一作者单位脑与认知科学国家重点实验室
推荐引用方式
GB/T 7714
Xu, Ya-Jie,Qiang, Min,Zhang, Jin-Ling,et al. Reactive carbonyl compounds (RCCs) cause aggregation and dysfunction of fibrinogen[J]. PROTEIN & CELL,2012,3(8):627-640.
APA Xu, Ya-Jie,Qiang, Min,Zhang, Jin-Ling,Liu, Ying,He, Rong-Qiao,&He, RQ .(2012).Reactive carbonyl compounds (RCCs) cause aggregation and dysfunction of fibrinogen.PROTEIN & CELL,3(8),627-640.
MLA Xu, Ya-Jie,et al."Reactive carbonyl compounds (RCCs) cause aggregation and dysfunction of fibrinogen".PROTEIN & CELL 3.8(2012):627-640.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
WOS_000310531900009.(1124KB)期刊论文出版稿限制开放CC BY-NC-SA请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Xu, Ya-Jie]的文章
[Qiang, Min]的文章
[Zhang, Jin-Ling]的文章
百度学术
百度学术中相似的文章
[Xu, Ya-Jie]的文章
[Qiang, Min]的文章
[Zhang, Jin-Ling]的文章
必应学术
必应学术中相似的文章
[Xu, Ya-Jie]的文章
[Qiang, Min]的文章
[Zhang, Jin-Ling]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。