iTRAQ analysis of a mouse acute myocardial infarction model reveals that vitamin D binding protein promotes cardiomyocyte apoptosis after hypoxia.
iTRAQ analysis of a mouse acute myocardial infarction model reveals that vitamin D binding protein promotes cardiomyocyte apoptosis after hypoxia.
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小鼠急性心肌梗死模型的 iTRAQ 分析揭示维生素 D 结合蛋白促进缺氧后心肌细胞凋亡
DOI:
10.18632/oncotarget.23025
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发表时间:
2018-01-05
期刊:
影响因子:
--
通讯作者:
Ma YT
中科院分区:
文献类型:
--
作者:
Wu Y;Liu F;Ma X;Adi D;Gai MT;Jin X;Yang YN;Huang Y;Xie X;Li XM;Fu ZY;Chen BD;Ma YT
The proteome profile changes after acute myocardial infarction (AMI) and the roles played by important protein species remain poorly understood. Here, we constructed a mouse AMI model by ligating the left coronary artery of male C57B/6J mice to investigate the molecular changes after AMI on the protein level. Total proteins of the left ventricle were extracted and quantitatively analyzed by isobaric tags using relative and absolute quantitation (iTRAQ) technologies. The transcript and protein levels of important genes were further validated using quantitative polymerase chain reaction and western blot. An oxygen and glucose deprivation/reperfusion cell model was constructed using H9C2 cells to further validate the expression patterns and functions of important proteins after hypoxia. Seven hundred seventy-six proteins were identified as differentially abundant proteins after AMI, of which 406 were accumulated, and 370 were reduced. Gene ontology enrichment analysis showed that the most enriched molecular function category terms were binding, including calcium ion biding, GTP binding, actin binding and lipid binding. The expression levels of vitamin D binding protein (VDBP) and its related proteins were increased in both left ventricular tissue and H9C2 cells after ischemia-hypoxia. Overexpression of VDBP in H9C2 cells reduced vitamin D receptor and promoted the cell apoptosis rate after hypoxia. Our data provided new insights into proteome profile changes after AMI and indicated that VDBP could promote cardiomyocyte apoptosis after hypoxia.
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DOI:
10.1074/mcp.m114.040675
发表时间:
2014-10
期刊:
Molecular & cellular proteomics : MCP
影响因子:
--
作者:
Peng Y;Gregorich ZR;Valeja SG;Zhang H;Cai W;Chen YC;Guner H;Chen AJ;Schwahn DJ;Hacker TA;Liu X;Ge Y
通讯作者:
Ge Y
影响因子:
2.5
作者:
Oda T;Matsumoto K
通讯作者:
Matsumoto K
影响因子:
1.1
作者:
Asadi H;Abolfathi AA;Badalzadeh R;Majidinia M;Yaghoubi A;Asadi M;Yousefi B
通讯作者:
Yousefi B
DOI:
10.1097/00000433-200203000-00017
发表时间:
2002-03-01
影响因子:
1
作者:
Hutchins, KD;Skurnick, J;Natarajan, GA
通讯作者:
Natarajan, GA
影响因子:
14.9
作者:
Du Z;Zhou X;Ling Y;Zhang Z;Su Z
通讯作者:
Su Z