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

Taniguchi, Kazumi; Satô, Noboru; Uchiyama, Yasuo

doi:10.1679/aohc.58.191

Cited by 56 publications

(38 citation statements)

References 20 publications

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“…In contrast to the few studies of the lip fusion process, the fate of the medial edge epithelial (MEE) cells of the secondary palatal shelves, which form the midline epithelial seam upon palatal shelf adhesion, has been studied extensively although considerable disagreement still exists. TEM and cell biological studies have provided clear evidence of apoptosis of at least a portion of the MEE cells (Glucksmann, 1965;Saunders, 1966;DeAngelis and Nalbandian, 1968;Smiley and Dixon, 1968;Shapiro and Sweney, 1969;Smiley and Koch, 1975;Mori et al, 1994;Taniguchi et al, 1995;Cuervo et al, 2002;Cuervo and Covarrubias, 2004). Others, however, reported that the midline epithelial seam cells looked healthy at the TEM level and found evidence of transdifferentiation of MEE cells into mesenchymal cells by using various cell labeling techniques (Fitchett and Hay, 1989;Shuler et al, 1991Shuler et al, , 1992Griffith and Hay, 1992;Sun et al, 1998;Martinez-Alvarez et al, 2000;Nawshad et al, 2004).…”

Section: Is Programmed Cell Death Emt or Both The Mechanism Involvementioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

288

304

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The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. Recent studies of craniofacial development in animal models have identified components of several major signaling pathways, including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial morphogenesis and/or lip fusion. There is also accumulating evidence that these signaling pathways cross-regulate genetically as well as crosstalk intracellularly to control cell proliferation and tissue patterning. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development and discuss the complex interactions of the various signaling pathways and challenges for understanding cleft lip pathogenesis.

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Section: Is Programmed Cell Death Emt or Both The Mechanism Involvementioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

288

304

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“…Migration of MEE cells towards the nasal and oral regions has also been proposed to participate in shelf fusion (Carette and Ferguson, 1992). Cell death, which has been known for many years to occur in the developing palate (DeAngelis and Nalbandian, 1968;Farbman, 1968;Smiley and Dixon, 1968), was until only recently implicated in MES degeneration (Cuervo et al, 2002;Martinez-Alvarez et al, 2000;Mori et al, 1994;Taniguchi et al, 1995). MES degeneration could also result from a combination of cellular mechanisms such as those described above.…”

Section: Introductionmentioning

confidence: 99%

Death is the major fate of medial edge epithelial cells and the cause of basal lamina degradation during palatogenesis

2004

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During mammalian development, a pair of shelves fuses to form the secondary palate, a process that requires the adhesion of the medial edge epithelial tissue (MEE) of each shelf and the degeneration of the resulting medial epithelial seam (MES). It has been reported that epithelialmesenchymal transformation (EMT) occurs during shelf fusion and is considered a fundamental process for MES degeneration. We recently found that cell death is a necessary process for shelf fusion. These findings uncovered the relevance of cell death in MES degeneration; however, they do not discard the participation of other processes. In the present work, we focus on the evaluation of the processes that could contribute to palate shelf fusion. We tested EMT by traditional labeling of MEE cells with a dye, by infection of MEE with an adenovirus carrying the lacZ gene, and by fusing wild-type shelves with the ones from EGFP-expressing mouse embryos. Fate of MEE labeled cells was followed by culturing whole palates, or by a novel slice culture system that allows individual cells to be followed during the fusion process. Very few labeled cells were found in the mesenchyme compartment, and almost all were undergoing cell death. Inhibition of metalloproteinases prevented basal lamina degradation without affecting MES degeneration and MEE cell death. Remarkably, independently of shelf fusion,activation of cell death promoted the degradation of the basal lamina underlying the MEE (`cataptosis'). Finally, by specific labeling of periderm cells (i.e. the superficial cells that cover the basal epithelium), we observed that epithelial triangles at oral and nasal ends of the epithelial seam do not appear to result from MEE cell migration but rather from periderm cell migration. Inhibition of migration or removal of these periderm cells suggests that they have a transient function controlling MEE cell adhesion and survival, and ultimately die within the epithelial triangles. We conclude that MES degeneration occurs almost uniquely by cell death, and for the first time we show that this process can activate basal lamina degradation during a developmental process.

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“…Earlier studies provided ultrastructural evidence for the occurrence of programmed cell death (PCD) in disappearing MEE cells such as the presence of autophagic vacuoles, lysosomes and macrophages (Shapiro and Sweney, 1969;Smiley, 1970;Smiley and Koch, 1975). The mode of cell death was shown to be apoptosis by cytochemical evidence of apoptotic DNA fragmentation (Mori et al, 1994;Taniguchi et al, 1995;Martínez-Álvarez et al, 2000;Cuervo et al, 2002;Cuervo and Covarrubias, 2004). On the other hand, Fitchett and Hay (1989) reexamined the process of palatal fusion in rats and observed the occurrence of epithelial-mesenchymal transformation (EMT) in the disappearing midline epithelial seam.…”

Section: Introductionmentioning

confidence: 99%

Terminal differentiation of palatal medial edge epithelial cells in vitro is not necessarily dependent on palatal shelf contact and midline epithelial seam formation

Takigawa

Shiota²

2004

Int. J. Dev. Biol.

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During fusion of the mammalian secondary palate, it has been suggested that palatal medial edge epithelial (MEE) cells disappear by means of apoptosis, epithelial-mesenchymal transformation (EMT) and epithelial cell migration. However, it is widely believed that MEE cells never differentiate unless palatal shelves make contact and the midline epithelial seam is formed. In order to clarify the potential of MEE cells to differentiate, we cultured single (unpaired) palatal shelves of ICR mouse fetuses by using suspension and static culture methods with two kinds of gasmixtures. We thereby found that MEE cells can disappear throughout the medial edge even without contact and adhesion to the opposing MEE in suspension culture with 95% O 2 /5% CO 2 . Careful examination of MEE cell behavior in the culture revealed that apoptosis, EMT, and epithelial cell migration all occurred at various stages of MEE cell disappearance, including the transient formation and disappearance of epithelial triangles and islets. In contrast, MEE cells showed poor differentiation in static culture in a CO 2 incubator. Furthermore, mouse and human amniotic fluids were found to prevent MEE cell differentiation in the cultured single palatal shelf, although paired palatal shelves fused successfully even in the presence of amniotic fluid. We therefore conclude that terminal differentiation of MEE cells is not necessarily dependent on palatal shelf contact and midline epithelial seam formation, but such MEE cell differentiation appears to be prevented in utero by amniotic fluid unless palatal shelves make close contact and the midline epithelial seam is formed.

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

Cited by 56 publications

References 20 publications

Development of the upper lip: Morphogenetic and molecular mechanisms

Development of the upper lip: Morphogenetic and molecular mechanisms

Death is the major fate of medial edge epithelial cells and the cause of basal lamina degradation during palatogenesis

Terminal differentiation of palatal medial edge epithelial cells in vitro is not necessarily dependent on palatal shelf contact and midline epithelial seam formation

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