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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: J Mol Cell Cardiol. 2014 Nov 13;79:133–144. doi: 10.1016/j.yjmcc.2014.11.003

Figure 1. Cyclic stretch increases EMCM proliferation, size, cardiac gene expression, and myofibrillar protein levels.

Figure 1

A. EDU staining comparing the proliferation rates of static and stretched EMCMs. Stretched EMCMs have a 21.3% increase in relative proliferation compared to static controls (1.21 +/− 6% vs. 1 +/− 3.2%; p<0.001; n=8–9). B. EMCMs exposed to stretch are 33% larger compared to static controls as quantified by flow cytometry (1.42×106 +/− 0.01 vs 1.07×106 +/− 0.04; p<0.001; n=3). C. qPCR for key cardiac genes demonstrates increased expression in stretched EMCMs compared to static controls. Gapdh was used as control. n=4–6. D. Immunoblotting showing representative total sarcomeric myosin heavy chain expression and Titin isoform levels. Total myosin heavy chain levels are increased in stretched EMCMs. Titin N2BA is the predominate isoform in stretched EMCMs, as compared to Titin N2B as is seen in static controls. E. Stretched EMCMs have increased Myosin heavy chain levels (1.38 +/− 0.10 vs 1 +/− 0.03; p=0.014; n=4). F. Quantification of Titin isoforms. 80.8% +/− 8.6% of Titin in stretched EMCMs is of the N2BA isoform. In contrast, static cardiomyocytes contain 22.8% +/− 9.4% of the Titin N2BA isoform. (the rest is Titin N2B; n=4; *p<0.05, **p<0.005, ^p<0.001).