Normal stages of cardiac organogenesis in the mouse: I. Development of the external shape of the heart

Vuillemin, Mauricette; Pexieder, Tomáš

doi:10.1002/aja.1001840202

Cited by 48 publications

(15 citation statements)

References 23 publications

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“…These transitional zones are detected in the same positions as those where we observed the epicardial rings. The external shape of the embryonic mouse heart develops differently from that of the chick (Vuillemin and Pexieder 1989). We speculate that the spreading epicardial cells have more affinity for these intersegmental grooves than for the myocardium of the cardiac segments.…”

Section: Discussionmentioning

confidence: 85%

Cytokeratins as a marker for epicardial formation in the quail embryo

et al. 1995

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Several techniques have been used to visualize the migration pattern of the epicardial cells from the proepicardial organ over the myocardial surface. As the epicardial cells contain keratin tonofilament bundles, we have incubated 92 whole-mount quail hearts with an anti-keratin antibody. This immunohistochemical method showed that the complete epicardial covering of the embryonic heart is preceded by the formation of three epicardial rings. The epicardial rings are formed on the outer myocardial surface in the grooves that separate the cardiac segments from each other. We have also documented timing and patterning of isolated epicardial islands. They are not encountered at random over the myocardial surface, but only along the edge of the advancing epicardial front border and in two defined future epicardial ring areas on the ventral side of the outflow tract. The epicardial islands suggest that in the quail free-floating parts of epicardium can attach to the myocardium. Characteristics of the surface of the myocardium at the transitional zones between the cardiac segments, as well as the three-dimensional remodelling of the heart during cardiac morphogenesis seem to play a role in the pattern in which the epicardium eventually completely ensheaths the myocardial surface. Congenital heart defects are often related to malpositioned transitional zones that dictate the pattern of epicardial outgrowth. As the embryonic position of the epicardial rings is mirrored in the pattern of the main arterial stems, the coronary vascularization pattern might be altered in congenitally malformed hearts as well.

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Section: Discussionmentioning

confidence: 85%

Cytokeratins as a marker for epicardial formation in the quail embryo

et al. 1995

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“…In a normal E8.5 embryo, the heart tube begins to bend with only the primitive ventricle discernible (Vuillemin and Pexieder, 1989). After E8.5 embryos were cultured for 48 hr, we observed that they developed into E9.5-like embryos (n ϭ 15).…”

Section: Effects Of Rock Inhibition On Cardiac Morphogenesismentioning

confidence: 82%

“…To further investigate the effects of ROCK inhibition in cardiac chamber development, we cultured E9.5 embryos, in which the primitive atrium, ventricle, and conotruncus have already formed (Vuillemin and Pexieder, 1989). After 48 hr of culture, the E9.5 control embryos developed into E10.5-like embryos (n ϭ 12).…”

Section: Effects Of Rock Inhibition On Cardiac Morphogenesismentioning

confidence: 99%

Rho‐associated kinases play an essential role in cardiac morphogenesis and cardiomyocyte proliferation

Zhao

Rivkees

2002

Developmental Dynamics

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Rho-associated coiled-coil kinases (ROCKs), initially identified as effectors for Rho GTPases, play a role in cardiac cell physiology and are also expressed in the developing heart. However, their role in cardiac development is not known. To investigate the role of these kinases in cardiac development, we examined cardiac development in cultured murine embryos treated with the ROCK inhibitor Y27632. After inhibition of ROCK activity, we found disturbed cardiac chamber formation and trabeculation. To further examine the mechanisms by which ROCK blockade causes cardiac hypoplasia, we assessed programmed cell death and cell proliferation in the hearts. We found decreased cell proliferation in the Y27632-treated hearts, but no changes in programmed cell death. We further observed that ROCK inhibition decreased cardiac myocyte proliferation, suggesting that ROCK kinases regulate cardiomyocyte division. To identify factors involved in ROCK action in regulation of cardiac cell division, we examined expression of cell cycle proteins by using Western blot analysis. We found that ROCK blockade decreased expression of cell cycle proteins, cyclin D3, CDK6, and p27 KIP1 in the hearts and cardiomyocytes, which are required for initiation of cell cycle and G1/S phase transition. These observations show that ROCK kinases play a role in cardiac development and that ROCK kinases regulate cardiac cell proliferation and cell cycle protein expression. Developmental Dynamics 226:24 -32, 2003.

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“…In the mouse, the left ventricle and right ventricle are discernible at E9.5 and E11.5, respectively (Vuillemin and Pexieder, 1989a). From E12.5 to E13.5, the right ventricle grows larger than the left ventricle, and this relationship persists throughout embryonic development (Vuillemin and Pexieder, 1989a).…”

Section: Discussionmentioning

confidence: 98%