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. 2013 Nov 23;4:11–17. doi: 10.1016/j.fob.2013.11.002

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© 2014 The Authors

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig. 1 — Significant expression of α-SMA in cTnI-ND mouse heart. Ventricular muscle homogenates of wild type, cTnI-ND, and cTnI-K118C (a double transgenic line expressing a cTnI mutant on the endogenous cTnI gene knockout background [13]) mice (∼80 μg total protein/lane), or mouse bladder (∼5 μg total protein/lane) were analyzed by SDS–PAGE (upper panel, Coomassie blue protein stain) and immunoblotting (lower three panels). The results detected a significant level of α-SMA in cTnI-ND hearts but not in the wild type and cTnI-118C control hearts. Smooth muscle-specific protein markers h1 and h2 calponins (RAH2 blot) and SM22 were examined as controls.