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.