Skip to main content
. Author manuscript; available in PMC: 2012 Nov 25.
Published in final edited form as: J Mol Cell Cardiol. 2005 Oct 19;39(6):865–873. doi: 10.1016/j.yjmcc.2005.09.007

Fig. 7.

Fig. 7

IGF stimulation of human ES cell-derived cardiomyocyte proliferation is mediated via PI 3-kinase. H7 human ES cells were differentiated for 21 days before Percoll separation, and fraction IV cells were cultured for an additional 4 days in serum-free media with various treatments for the final 48 hours of culture prior to fixation. The PI 3-kinase inhibitor LY294002 significantly inhibited and IGF-1 significantly stimulated hESC-derived cardiomyocyte proliferation (** = P < 0.01 and * = P < 0.05, respectively), similar to previous results. Dual treatment with IGF-1 and LY294002 significantly inhibited proliferation (P < 0.05) compared to treatment with IGF-1 alone, suggesting that IGF-1 stimulated proliferation is mediated via the PI 3-kinase pathway.

HHS Vulnerability Disclosure