Early heart development in the chick embryo: effects of isotretinoin on cell proliferation, α-actin synthesis, and development of contractions

Wiens, Darrell J.; Mann, Tamara K.; Fedderson, Dan E.; Rathmell, W. Kimryn; Franck, Barbara H.

doi:10.1111/j.1432-0436.1992.tb00686.x

Cited by 24 publications

(16 citation statements)

References 49 publications

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“…In regards to apoptosis, there was no evidence of dying cells within the newly formed mesenchyme, myocardium or endothelium suggesting that the decrease in cell number was not due to cell death caused by RA. This is consistent with other investigators, who reported no evidence of cell death using the same concentration of RA (Wiens et al, 1992;Dickman and Smith, 1996). Because we did not specifically test for apoptosis, however, we can not completely rule out this process as contributing to the decrease in mesenchyme cells.…”

Section: Discussionsupporting

confidence: 91%

“…RA may either increase or decrease the differentiation of myocardium (Drysdale et al, 1997;Kastner et al, 1997). Studies have also reported that RA inhibits cardiac myocyte proliferation, development of heart contractions and ␣-actin synthetic rate (Wiens et al, 1992;Dickman and Smith, 1996). Finally, myocardial differentiation markers in Xenopus embryos are blocked upon exposure to RA, whereas the pattern of endocardial gene expression remained unaffected (Drysdale et al, 1997).…”

Section: Discussionmentioning

confidence: 97%

“…RA administration has been associated with inhibiting neural crest cell migration and with increasing apoptosis. These could also account for the decrease in mesenchymal cells within the cushion (Hart et al, 1990;Wiens et al, 1992). Although RA administration may inhibit neural crest migration into outflow tract cushions, however, this study deals only with the AV cushions that are devoid of neural crest cells.…”

Section: Discussionmentioning

confidence: 99%

“…There are a number of theories on the mechanism responsible for these defects. These include interference with cranial neural crest migration; direct cytotoxicity of RA on cardiac cells; increasing apoptosis of myocardial cells; and alteration of the production of ECM components (Taylor et al, 1980;Davis and Sadler, 1981;Kato and De Luca, 1987;Hart et al, 1990Hart et al, , 1992Wiens et al, 1992;Nakajima et al, 1997;Bouman et al, 1998). Using co-cultures of endocardium with myocardium from mouse embryonic hearts in collagen gels, Nakajima (Nakajima et al, 1996) showed that maternally administered RA suppressed cushion mesenchyme formation and that this suppression could be reversed by the addition of MyoCM.…”

Section: Discussionmentioning

confidence: 99%

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Retinoic acid administration is associated with changes in the extracellular matrix and cardiac mesenchyme within the endocardial cushion

Yan

Sinning

2001

Anat. Rec.

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Retinoic acid has been associated with a number of cardiac defects, some of which seem to be related to changes in the endocardial cushions. Studies in mice and older chick embryos have suggested that these defects may be associated with a decrease in mesenchymal cell formation within the cushion. In a previous report we showed that retinoic acid lowered the number of mesenchymal cells in a culture bioassay of mesenchyme formation and that this response was due to retinoic acid modifying the production of particulate matrix from the myocardium. In this study, we have extended these observations to the embryo by implanting a retinoic acid coated bead into the embryo and examined the effect on cardiac mesenchyme formation and in the production of the particulate matrix. In all cases the addition of retinoic acid resulted in a decrease in the number of mesenchymal cells invading the endocardial cushions. In addition retinoic acid increased the production of hLAMP-1 and fibronectin but not transferrin, confirming our earlier report. Finally, we measured the volume of the cushion and calculated the cell density of both the inferior and superior cushions. The results suggest that the superior cushion is more sensitive to retinoic acid treatment than the inferior cushion. Collectively, these results support our earlier work that suggests that the mechanism of retinoic acid cardiac abnormalities involves a disruption in the production of particulate matrix from the myocardium and a subsequent decrease in cardiac mesenchyme cells that results in a malformed cardiac cushions. Anat Rec 263: [53][54][55][56][57][58][59][60][61] 2001.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Retinoic acid administration is associated with changes in the extracellular matrix and cardiac mesenchyme within the endocardial cushion

Yan

Sinning

2001

Anat. Rec.

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“…A greater sensitivity of the right side of the heart to toxic agents has already been described by Hyman (1927). When the right ventricular myocardium would be sensitive to retinoic acid, which inhibits myocardial cell proliferation (Wiens et al, 1992), this could be based on the fact that before cardiac septation myocardial growth is accelerated in the right ventricle when compared to the left ventricle . Until now, no other effects of retinoic acid on the myocardium have been suggested.…”

Section: Direct Effects Of Retinoic Acidmentioning

confidence: 99%

Stereological study of stage 34 chicken hearts with looping disturbances after retinoic acid treatment: Disturbed growth of myocardium and atrioventricular cushion tissue

Bouman¹,

Broekhuizen²,

Baasten³

et al. 1997

Anat. Rec.

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Background: In a previous study retinoic acid treatment of chicken hearts has resulted in a spectrum of looping disturbances. Because of a decrease in contraction force of these hearts, the myocardial volume was hypothesized to be altered. Because retinoic acid has been suggested to influence endocardial cushion volumes, these were estimated as well.Methods: The previously studied hearts were used for estimating the absolute volumes of the atrial and ventricular myocardium and of the endocardial cushions by means of Cavalieri's principle. To measure the surface density of the trabeculations according to the isector method, we used retinoic acid treated hearts, which were perfusion fixed and in which the sections were isotropic uniform random. The volumes and surface densities found in the three morphologically distinguished groups, i.e., intact septum, isolated ventricular septal defect and double outlet right ventricle, were compared with those in shams.Results: A significant volume decrease was found in the right ventricular free wall myocardium of the double outlet right ventricle. No significant differences were found in the surface densities of the trabeculae. The volume of the atrioventricular cushion tissue in the double outlet right ventricle hearts was significantly increased. The morphological spectrum observed previously was also expressed in the right ventricular myocardial volume, which appeared to decrease from the least to the most malformed hearts, and in the volume of the atrioventricular cushion tissue, which appeared to increase.Conclusions: Several studies have shown pathology in myocardial and cushion tissue after retinoic acid treatment. In this study we have found a decreased growth of the right ventricular myocardium and an increased growth of the atrioventricular cushion tissue. We suggest that the previously found looping disturbance causes changed hemodynamics, as reported elsewhere, and that these result in changes in growth. We cannot exclude a direct effect of retinoic acid on the myocardium, which has to explain the looping disturbance. Anat.

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Selective regulation of cardiomyocyte gene expression and cardiac morphogenesis by retinoic acid

Dickman

Smith

1996

Dev. Dyn.

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Early heart development in the chick embryo: effects of isotretinoin on cell proliferation, α-actin synthesis, and development of contractions

Cited by 24 publications

References 49 publications

Retinoic acid administration is associated with changes in the extracellular matrix and cardiac mesenchyme within the endocardial cushion

Retinoic acid administration is associated with changes in the extracellular matrix and cardiac mesenchyme within the endocardial cushion

Stereological study of stage 34 chicken hearts with looping disturbances after retinoic acid treatment: Disturbed growth of myocardium and atrioventricular cushion tissue

Selective regulation of cardiomyocyte gene expression and cardiac morphogenesis by retinoic acid

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