Abstract
Di-peptidyl peptidase 4 (DPP-4) is a membrane spanning exopeptidase that cleaves dipeptides from the N terminus of proteins/peptides. Recent studies demonstrate circulating DPP-4 activity is increased in diabetes, which may in part explain the poor prognosis of diabetic patients with ischemic heart disease. In addition to degrading glucagon-like peptide-1 (GLP-1), DPP4 is also known to degrade stromal derived factor-1 (SDF-1), a pro-angiogenic and cardiomyocyte protective protein currently in early phase clinical trials for patients with ischemic heart disease. We hypothesized that DPP-4 inhibition in the diabetic post myocardial infarction (MI) setting may confer a benefit as a result of enhanced SDF-1 availability rather than potentiating GLP-1. We therefore compared DPP-4 inhibition with GLP-1 agonism, and used the specific SDF-1 receptor (CXCR4) antagonist, AMD3100 to demonstrate SDF-1 specificity.
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