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. 2009 May 18;4(5):e5589. doi: 10.1371/journal.pone.0005589

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Chen et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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A. Haematoxylin-eosin staining showed slightly distorted and wavy myofibers in Mecr transgenic hearts (a1 and a2). There is no significant difference in heart weight/body weight between wild type and Mecr transgenic mice (a3). Toluidine blue staining showed an uneven staining pattern in transgenic cardiomyocytes (a4 and a5). The diameter of myofibers was greater in transgenic heart than in wild type (SD (n = 6) ***P<0.001) (a6). TUNEL staining showed an increased number of positively stained nuclei (SD (n = 5) **P<0.005) in Mecr transgenic mice vs. controls (a7 through a9). B. Transmission electron micrographs show well-organized myofibrils and regularly located mitochondria in wild type hearts (b1), whereas in Mecr transgenic hearts myofibrils are disorganized (b2). Accumulated mitochondria and a few degenerating organelles can be also seen (b3). High-density cristae were only observed in transgenic mitochondria (b4). b5 shows an enlargement of the indicated area in b4. The average diameter of mitochondria is larger in Mecr transgenic mice than in wild type controls (SD (n = 6) ***P<0.001) (b6). Bars represent 1 µm (b1–b3) and 200 nm (b4), respectively. “m” represents mitochondrion. The arrows show distorted myofibrils; the arrow heads point to degenerated mitochondrion.