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Figure 3 Pre-Treatment of MSCs With GFs Potentiated Their Cytoprotective Effects on CMCs, Which Was Mediated Through Gap Junction
(A to D) Fluorescence-activated cell sorter (FACS) for evaluating apoptosis. The CMCs were exposed to hypoxia alone as a control (A), under coculture with untreated MSCs (B), and GF-treated MSCs (C). Hypoxia-induced apoptosis of CMCs was reduced by coculture with MSCs, which was more notable in coculture condition with GF-treated MSCs. Heptanol partially inhibited cytoprotective effects of GF-treated MSCs on CMCs (D). (E) Western blot analysis. The expression of phospho-Akt (p-Akt) and phospho-c-AMP response element binding protein (p-CREB) increased in CMCs cocultured with GF-treated MSCs under hypoxia, which was reversed by gap junctional blocker. (F) Enzyme-linked immunosorbent assay (ELISA) for insulin-like GF (IGF)-1 and hepatocyte GF (HGF). There was no significant difference in secretion of IGF-1 and HGF between untreated and GF-treated MSCs. Abbreviations as in Figure 1.
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