iTRAQ analysis of a mouse acute myocardial infarction model reveals that vitamin D binding protein promotes cardiomyocyte apoptosis after hypoxia
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Yun Wu1,3,*, Fen Liu1,*, Xiang Ma1,2, Dilare Adi1,2, Ming-Tao Gai1, Xiang Jin1,4, Yi-Ning Yang1,2, Ying Huang1,2, Xiang Xie1,2, Xiao-Mei Li1,2, Zhen-Yan Fu1,2, Bang-Dang Chen2 and Yi-Tong Ma1,2
1Xinjiang Key Laboratory of Cardiovascular Disease Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, P.R. China
2Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, P.R. China
3Department of General Practice, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, P.R. China
4Proteomics Research Center, Ruikangda Medical Research Institution, Urumqi 830063, P.R. China
*These authors contributed equally to this work
Yi-Tong Ma, email: firstname.lastname@example.org
Keywords: acute myocardial infarction; quantitative proteomics; isobaric tags for relative and absolute quantitation; vitamin D binding protein
Received: May 17, 2017 Accepted: September 03, 2017 Published: December 06, 2017
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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