Palatal fusion in vitro in the mouse

Vargas, Victor Ignacio Cruz

doi:10.1016/0003-9969(67)90130-6

Cited by 37 publications

(16 citation statements)

References 5 publications

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“…By the time that the two palatal shelves become identifiable as bilateral projections from the maxillary processes, they already have cells containing the information €or palatal differentiation which can be expressed normally under appropriate in vitro conditions. This is in agreement with the conclusions of Tyler and Koch (1975); the findings of certain other investigators (Pourtois, 1966(Pourtois, , 1972Vargas, 1967) were likely caused by differences in their culture systems (Smiley and Koch, 1975).…”

Section: Discussionsupporting

confidence: 91%

“…The present study also negates the idea that palatal shelves acquire a "potential for fusion" under the influence of undescribed in vivo conditions (Pourtois, 1966(Pourtois, , 1972Vargas, 1967). For the mouse it was reported (Pourtois, 1966(Pourtois, , 1972Vargas, 1967) that prior to 13.5 days, palatal shelves are "not fully predifferentiated" and so are unable to fuse if explanted into culture before this time. Results from the present study, however, indicate that palatal shelves from 17); instead only an occasional dead epithelial cell is stained farrows).…”

Section: Discussioncontrasting

confidence: 81%

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Differentiation of cultured palatal shelves from alligator, chick, and mouse embryos

1984

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Palatal shelves from embryonic alligators, chicks, and mice were explanted at various stages of development and organ cultured in either chemically defined, serumless media or the same media supplemented with 10% fetal calf serum. Shelves from each vertebrate were either cultured singly or in contact, and heterologous combinations of palatal shelves from different animals were made: chick/mouse, chick/alligator, and mouse/alligator. Epithelial differentiation (particularly that of the medial shelf edge) was assayed by vital staining, histology, and scanning electron microscopy. In vitro medial edge epithelial differentiation, and consequently the mechanisms of palatal closure, were identical to those normally seen in vivo for each species, i.e., cobble-stoned migrating epithelia in the alligator, cell death and fusion in the mouse, and keratinisation and cleft palate in the chick. Differentiation was optimal in the chemically defined, serumless media and was independent of shelf contact in all three species. No heterologous combinations of palatal shelves closed with each other: Evidently, the modes of palatal closure in mice and alligators are sufficiently different to prevent them forming a chimeric palate, whilst neither is capable of inducing closure in a cocultured chick palatal shelf. These unified defined culture conditions make possible a large number of epithelial-mesenchymal recombination studies as well as specific inhibitor, teratogenic, and hormonal investigations.

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Section: Discussionsupporting

confidence: 91%

Section: Discussioncontrasting

confidence: 81%

Differentiation of cultured palatal shelves from alligator, chick, and mouse embryos

1984

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“…In the late 1960s, scientists using palate organ culture models to study palatogenesis reported that palatal shelves acquired a potential to fuse that was restricted to specific developmental stages (Purtois, 1966;Vargas, 1967). The palate organ culture model eliminated shelf elevation as a factor and allowed evaluation of biological processes necessary for fusion.…”

Section: Observations Stimulating An Interest In Fusion Events As a Tmentioning

confidence: 98%

The etiology of cleft palate: a 50‐year search for mechanistic and molecular understanding

Abbott

2010

Birth Defects Research Pt B

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Dates of special, historical significance, such as the 50th anniversary of the founding of the Teratology Society, prompt a desire to pause and look back and contemplate where we began, how far we have come, and consider the future for our scientific endeavors. The study of the etiology of cleft palate extends many years into the past and was a subject of interest to many of the founding members of the Teratology Society. This research area was intensively pursued and spawned a vast portfolio of published research. This article will look back at the state of the science around the time of the founding of the Teratology Society, in the 1950s and 1960s, and track the emergence and pursuit of an interest in an etiology for cleft palate involving failure of palatal fusion. Studies of medial epithelial cell fate and induction of cleft palate by interference with adhesion or fusion span the period from the 1960s to the present time. Teratology Society members have been and continue to be key players in cleft palate research. In this retrospective article, seminal research published by Teratology Society members will serve as a platform to launch the discussion of the emergence of our current understanding of medial epithelial cell differentiation and fate and the potential for these processes to be targets of teratogenic action.

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“…The potential of the palatal shelves to fuse in vitro depends on the age of embryo, which varies among species. Pourtois (1966) found that in the rat the potential to fuse was acquired 24 h before the actual time of the secondary palatal fusion, whereas Vargas (1967) found that in the mouse it was at least 40 h before the actual time of fusion in vivo. Teratogens that disturb any of these developmental …”

Section: Fig1 Hematoxylin and Eosin (H And E)-stained Sections Of The mentioning

confidence: 99%

“…Transplants were classified in three groups according to Vargas (1967) method: no fusion, partial fusion, and complete fusion. Complete fusion or mesenchymal coalescence means no MEE is observed, and the epithelial laminae have been broken down and resorbed.…”

Section: Light Microscopementioning

confidence: 99%

A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B12 on murine embryonic palatal shelf fusion in vitro

Wang

Shi

et al. 2008

J. Zhejiang Univ. Sci. B

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Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B 12 has been shown to antagonize the teratogenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B 12 on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on embryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B 12 . The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B 12 -treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B 12 group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B 12 prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.

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Palatal fusion in vitro in the mouse

Cited by 37 publications

References 5 publications

Differentiation of cultured palatal shelves from alligator, chick, and mouse embryos

Differentiation of cultured palatal shelves from alligator, chick, and mouse embryos

The etiology of cleft palate: a 50‐year search for mechanistic and molecular understanding

A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B12 on murine embryonic palatal shelf fusion in vitro

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