Fig. 2.

Molecular analysis of Wnt antagonism and related mechanisms in WJMSC-derived cardiomyocytes. a, b Wnt antagonists (sFRP1–5, Dkk 1 and 3) and Wnt-related genes (CreB, calcineurin (CalN), vinculin (VCL), and DDX20) were analyzed by semi-quantitative (A1, B1) and quantitative (A2, B2) RT-PCR for untreated and DC301 + DC302-treated WJMSCs (*p < 0.05, **p < 0.01, n = 3). c Calcium release for control and DC301 + DC302-treated WJMSCs was monitored by FURA2M staining (scale bars = 100 μm, n = 3). d Release of nitric oxide (NO) accompanying cardiac differentiation was studied by Griess assay for WJMSCs induced with DC301, DC302, and DC303, and various combinations of these inhibitors as indicated (*p < 0.05, **p < 0.01, n = 3). Schematic 1: representation of the development of cardiomyocytes from MSCs by epigenetic modification via Wnt mediators. Dkk Dickkopf, sFRP secreted frizzled-related protein, MSC mesenchymal stem cell