FIGURE 8.

Knockdown of CaMKIIδB does not impair commitment of CPCs toward the cardiac or smooth muscle phenotype. A, cardiac markers Mef2c; B, cardiac troponin T (tnnt3); and C, smooth muscle marker α-smooth muscle actin gene expression in CPC sh-Ctrl and CPC sh-δB during growth conditions and after the addition of dex. Values are represented as fold change mRNA relative to CPC sh-Ctrl in GM after normalizing to ribosomal 18. D, CPC sh-Ctrl and E, CPC sh-δB fluorescent images after staining for Mef2c protein. Cells were maintained in GM. Cells were stained with antibodies toward GFP to identify cells that were successfully transduced with the sh-based lentivirus. Cell morphology and nuclei were visualized by staining for tubulin and with DAPI, respectively. F, immunoblotting for α-smooth muscle actin in CPC sh-Ctrl and CPC sh-δB in GM, medium without dex, or medium with dex. G, quantitation of α-smooth muscle actin represented as a fold change relative to CPC sh-Ctrl in GM and after normalizing to GAPDH.