IGFBP3 and myocardial infarction: The cross-talk between MSC and ECFC and the ensuing modulated secretory activity observed in this study could possibly stimulate in vivo effects such as local angiogenesis (likely through VEGF, IGFBP-3, and YKL-40) [29,43], protection of cardiomyocytes against apoptosis (likely through IGFBP-3) [44], or prevention of left ventricular dilation post-MI (likely through OPN) [37].