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. Author manuscript; available in PMC: 2008 Oct 15.
Published in final edited form as: Dev Biol. 2007 Aug 9;310(2):291–303. doi: 10.1016/j.ydbio.2007.07.041

Figure 7. Thin myocardium syndrome is associated with reduced myocardial proliferation in the Crtl1-deficient mouse.

Figure 7

Panels A and B are hematoxylin-eosin stained sections of wild-type (A) and Crtl1−/− (B) specimens at ED13.0. The compact myocardium of the Crtl1−/− mouse has approximately half of the number of cell layers as compared to the compact myocardium in the wild type mouse (Panel B; thickness denoted by double-headed white arrows). PCNA labeling of wild type (C, E) and Crtl1−/− (D, F) ED13.0 specimens shows that the level of proliferation, expressed as PCNA-positive nuclei over total nuclei, is significantly reduced (t stat=4.34, p=0.02) in the ventricular wall of the Crtl1−/− specimens (white arrows D, F) when compared to wild type controls (C, E). However proliferation does not appear to be greatly affected in the interventricular septum (C, D, white star) or in the trabeculae (black arrows). LV=left ventricle, (*)= interventricular septum.