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Fig. 6 | Stem Cell Research & Therapy

Fig. 6

From: Insulin-like growth factor-II overexpression accelerates parthenogenetic stem cell differentiation into cardiomyocytes and improves cardiac function after acute myocardial infarction in mice

Fig. 6

IGF-II overexpression activated the IGF1R/INSR signaling in PSCs. a Western blot analysis determined the IGF1R, p-IGF1R, IGF2R, p-IGF2R, INSR, and p-INSR protein levels in cell derivatives at differentiation day 17. b Quantification of a. Data are presented as the fold change relative to pME 18s D3-derived cells (n = 8). c qRT-PCR was performed to detect IGF1R, IGF2R, and INSR mRNA expression in cell derivatives on day 17 (n = 8). Data were normalized to β-actin and were presented on a logarithmic scale as the fold change relative to pME 18s PSC-derived cells. d–i Cyclin D2 (brown) immunocytochemical analysis at day 24 in cell derivatives from pME 18s PSCs (d), pME 18s IGF-II-PSCs (e), pME 18s IGF-II-PSCs+control (ctr) shRNA (f), pME 18s IGF-II-PSCs+IGF-II shRNA (g), pME 18s PSCs+IGF-II (h), and pME 18s PSCs+IGF-II+IGF1R inhibitor (i). Nuclei were counterstained with hematoxylin. Scale bar, 25 μm. j The average optical density (OD) of the stained cells in d–i was detected and was presented on a logarithmic scale as the fold change relative to pME 18s PSC-derived cells (n = 8). k, l Western blotting analysis for cell derivatives in different groups as indicated (k) and quantitative analysis (l). Band intensities in (k) were quantified, and the protein expression level was presented as the fold change relative to pME 18s PSC-derived cells (n = 8). *p < 0.05 vs. pME 18s PSCs; ∆p < 0.05 vs. pME 18s IGF-II-PSCs+control shRNA; †p < 0.05 vs. pME 18s PSCs+IGF-II

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