VEGF Contributes to Mesenchymal Stem Cell-Mediated Reversion of Nor1-Dependent Hypertrophy in iPS Cell-Derived Cardiomyocytes

Figure 1

Characterization of hypertrophied iPS-CM. iPS-CM were cultured in the presence of 100 μM phenylephrine (PE) to induce hypertrophy. (a) Scatter plot of microarray data showing log2 of the gene transcripts between iPS-CM and iPS-CM treated with PE. (b) Top 30 up- and downregulated genes in PE-treated iPS-CM. Additional significantly upregulated genes involved in hypertrophic cell growth are highlighted by the dotted square. (c) Nor1 gene expression was verified by real-time PCR. . (d) Western blot analysis of Nor1 (), normalized to the expression levels of GAPDH. The expression of phosphorylated Akt (pAkt, ) and phosphorylated Erk (pERK, ) in hypertrophied iPS-CM was normalized to that of the unphosphorylated forms. (e) iPS-CM were seeded on fibronectin-coated coverslips and treated with 100 μM PE for 24 h. Cells were further fixed and incubated with Alexa Fluor 555 phalloidin to stain intracellular F-actin (red). Nuclei were counterstained with DAPI (blue), and the cell area was quantified microscopically. Bar: 100 μm; . , .

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