A radioautographic study of deoxyribonucleic acid synthesis in embryonic rat palatal shelf epithelium with reference to the concept of programmed cell death

Hudson, Carolyn D.; Shapiro, Burton L.

doi:10.1016/0003-9969(73)90022-8

Cited by 92 publications

(33 citation statements)

References 16 publications

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“…The classical hypothesis that cell death is required for palatogenesis has been proposed based on the observations as follows: (1) some MEE cells develop ultrastructural changes that are characteristic to dead cells prior to and/or during palatal fusion (Farbman,1968;Shapiro and Sweney, 1969;Chaudhry and Shah, 1973); (2) MEE cells cease DNA synthesis prior to the fusion of palatal shelves (Hudson and Shapiro, 1973;Pratt and Martin, 1975;Greene and Pratt, 1976); and (3) lysosomal enzyme levels in MEE cells increase prior to or during palatal fusion (Hayward, 1969;Smiley, 1970;Pratt and Greene, 1976). Furthermore, several morphological studies detected degenerated cells in the midline epithelial seam and among disappearing midline epithelial cells (Farbman, 1968;Hayward, 1969;Mato et al, 1972;Pratt and Hassel, 1975).…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that MEE cells cease incorporating 3 Hlabeled thymidine approximately 24 hours prior to initial contact of the opposing palatal shelves (Hudson and Shapiro, 1973;Pratt and Martin, 1975;Greene and Pratt, 1976). This phenomenon has been interpreted as a preparation of MEE cells to die.…”

Section: Discussionmentioning

confidence: 99%

“…However, there is disagreement as to whether MEE cell death occurs before or after the contact of palatal shelves. Cytological changes indicative of cell death such as ultrastructural changes of cell organelles, cessation of DNA synthesis and increased lysosomal levels have been observed in MEE cells prior to the contact of palatal shelves (Shapiro and Sweney, 1969;Smiley, 1970;Hudson and Shapiro, 1973;Greene and Pratt, 1976). On the other hand, using in situ labeling of DNA fragmentation, we previously detected a cytochemical evidence for apoptotic cell death occurring in the disappearing midline epithelial seam at some late stage of palatal fusion when the midline epithelial seam was disrupting, but not at earlier stages of palatogenesis (Mori et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Programmed cell death is not a necessary prerequisite for fusion of the fetal mouse palate.

Takahara

Takigawa²,

Shiota³

2004

Int. J. Dev. Biol.

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It has been widely accepted that programmed cell death (PCD) is an essential event in palatogenesis and that its failure can result in cleft palate, one of the most common birth defects in the human. However, some conflicting results have been reported concerning the timing of cell death occurring in the fusing palate and therefore the role of PCD in palatal fusion is controversial. In order to clarify whether cell death is indispensable for mammalian palatogenesis, we cultivated the palates of day-13 mouse fetuses in vitro and prevented cell death by treating them with the inhibitors of caspases-1 and -3 or with aurintricarboxylic acid which inhibits the activity of caspaseactivated DNase. Even when cell death was almost completely inhibited, palatal fusion took place successfully. Histological examination revealed that in the absence of apoptotic cell death, the medial edge epithelia of opposing palatal shelves adhered to each other and subsequently, the midline epithelial seam was disrupted and disappeared to bring about mesenchymal confluence across the palate. It seems that cell death is not a necessary prerequisite for palatal fusion but it may help to efficiently eliminate unnecessary cells which failed to migrate or differentiate properly.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Programmed cell death is not a necessary prerequisite for fusion of the fetal mouse palate.

Takahara

Takigawa²,

Shiota³

2004

Int. J. Dev. Biol.

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“…Programmed cell death of the MEE following the initial adherence of the palatal shelves was originally hypothesized (Shapiro and Sweney, 1969;Hudson and Shapiro, 1973;Pratt and Martin, 1975;Pratt and Greene, 1976;Pratt et al, 1984). The other two fates for the MEE were more recently proposed.…”

Section: Fate Of the Medial Edge Epitheliummentioning

confidence: 99%

Programmed Cell Death and Cell Transformation in Craniofacial Development

Shuler

1995

Critical Reviews in Oral Biology & Medicine

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Fusion of branchial arch derivatives is an essential component in the development of craniofacial structures. Bilaterally symmetric branchial arch processes fuse in the midline to form the mandible, lips, and palate. The mechanism for fusion requires several different morphologic and molecular events prior to the completion of the mesenchymal continuity between opposing tissue processes. The ectodermal covering of the branchial arches is one of the cell types that has an important role during craniofacial development. The surface epithelia provide the initial adherence between the processes; however, this population of cells is ultimately absent from the fusion zone. The medial edge epithelium of the secondary palatal shelves is one example of such an epithelium that must disappear from the fusion zone of the secondary palate during development in order to complete palatal fusion. The mechanisms for removal of the epithelial cells from the fusion zone could include either programmed cell death, epithelial-mesenchymal transformation, or migration to adjacent epithelia. All three of these fates have been hypothesized as a mechanism for the removal of the palatal medial edge epithelia. The processes of programmed cell death, epithelial-mesenchymal transformation, and epithelial migration are reviewed with respect to both palatal fusion and results reported in other model systems.

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“…Since no cell proliferation occurs in the medial edge epithelium (HUDSON and SHAPIRO, 1973), the palatal growth may result in the thinning of the seam and formation of the nasal and oral epithelial triangles and of the epithelial pearls. This may explain the reason why TUNEL-positive nuclei of MEE cells rarely appeared in the seam, as has been suggested by CARETTE and FERGUSON (1992), who have further reported that no degenerative cell appears in the triangles.…”

Section: Apoptosis Of Mee Cells During the Palatal Formationmentioning

confidence: 99%

Apoptosis and Heterophagy of Medical Edge Epithelial Cells of the Secondary Palatine Shelves During Fusion.

Taniguchi

Satô

Uchiyama

1995

Archives of Histology and Cytology

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A radioautographic study of deoxyribonucleic acid synthesis in embryonic rat palatal shelf epithelium with reference to the concept of programmed cell death

Cited by 92 publications

References 16 publications

Programmed cell death is not a necessary prerequisite for fusion of the fetal mouse palate.

Programmed cell death is not a necessary prerequisite for fusion of the fetal mouse palate.

Programmed Cell Death and Cell Transformation in Craniofacial Development

Apoptosis and Heterophagy of Medical Edge Epithelial Cells of the Secondary Palatine Shelves During Fusion.

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