Proteomic analysis of metabolic, cytoskeletal and stress response proteins in human heart failure.
Proteomic analysis of metabolic, cytoskeletal and stress response proteins in human heart failure.
复制标题
人类心力衰竭代谢、细胞骨架和应激反应蛋白的蛋白质组学分析
DOI:
10.1111/j.1582-4934.2011.01336.x
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发表时间:
2012-01
影响因子:
5.3
通讯作者:
Du J
中科院分区:
文献类型:
--
作者:
Li W;Rong R;Zhao S;Zhu X;Zhang K;Xiong X;Yu X;Cui Q;Li S;Chen L;Cai J;Du J
Human heart failure is a complex syndrome and a primary cause of morbidity and mortality in the world. However, the molecular pathways involved in the remodelling process are poorly understood. In this study, we performed exhaustive global proteomic surveys of cardiac ventricle isolated from failing and non‐failing human hearts, and determined the regulatory pathway to uncover the mechanism underlying heart failure. Two‐dimensional gel electrophoresis (2‐DE) coupled with tandem mass spectrometry was used to identify differentially expressed proteins in specimens from failing (n = 9) and non‐failing (n = 6) human hearts. A total of 25 proteins with at least 1.5‐fold change in the failing heart were identified; 15 proteins were up‐regulated and 10 proteins were down‐regulated. The altered proteins belong to three broad functional categories: (i) metabolic [e.g. NADH dehydrogenase (ubiquinone), dihydrolipoamide dehydrogenase, and the cytochrome c oxidase subunit]; (ii) cytoskeletal (e.g. myosin light chain proteins, troponin I type 3 and transthyretin) and (iii) stress response (e.g. αB‐crystallin, HSP27 and HSP20). The marked differences in the expression of selected proteins, including HSP27 and HSP20, were further confirmed by Western blot. Thus, we carried out full‐scale screening of the protein changes in human heart failure and profiled proteins that may be critical in cardiac dysfunction for future mapping.
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影响因子:
5
作者:
Fountoulakis, M;Soumaka, E;Capetanaki, Y
通讯作者:
Capetanaki, Y
DOI:
10.3109/13506120009146252
发表时间:
2000-06-01
期刊:
AMYLOID-INTERNATIONAL JOURNAL OF EXPERIMENTAL AND CLINICAL INVESTIGATION
影响因子:
--
作者:
Janunger, T;Anan, I;Tashima, K
通讯作者:
Tashima, K
影响因子:
3.4
作者:
Jin, X;Xia, L;Fang, NY
通讯作者:
Fang, NY
影响因子:
3.7
作者:
Lee HG;Chen Q;Wolfram JA;Richardson SL;Liner A;Siedlak SL;Zhu X;Ziats NP;Fujioka H;Felsher DW;Castellani RJ;Valencik ML;McDonald JA;Hoit BD;Lesnefsky EJ;Smith MA
通讯作者:
Smith MA
影响因子:
20.1
作者:
Fan, GC;Chu, GX;Kranias, EG
通讯作者:
Kranias, EG