Electron Microscopic and Histochemical Examination of Oral Epithelial-Mesenchymal Interaction (Programmed Cell Death)

Shapiro, Burton L.; Sweney, L. R.

doi:10.1177/00220345690480050801

Cited by 82 publications

(33 citation statements)

References 12 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

285

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

285

304

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“…During mammalian palate development, the initially vertically oriented palatal shelves are often in direct contact with but do not normally adhere to the mandible or the developing tongue (Shapiro and Sweney, 1969;Mato and Uchiyama, 1975;Ferguson et al, 1984). Pathological palatemandible and palate-tongue fusions, however, have been reported in humans, mice, and rats (Humphrey, 1970;Mato and Uchiyama, 1975;Shah, 1977;Jiang et al, 1998;Din, 2003;Alappat et al, 2005), suggesting that the competence for oral and palatal shelf adhesion must be spatiotemporally regulated.…”

Section: Introductionmentioning

confidence: 99%

“…Pourtois (1966) investigated the ability of different prefusion stage palatal shelves of rat embryos to fuse in explant cultures in vitro and concluded that a process of cellular differentiation occurs in the palatal shelves to acquire fusion competence during the stage of palatal shelf elevation in vivo. Electron microscopy studies showed that the prefusion palatal epithelium is composed of two layers of cells (Shapiro and Sweney, 1969;Fitchett and Hay, 1989). The surface layer consists of flat periderm cells, similar to the rest of the oral epithelia, and the basal layer consists of cuboidal ectoderm cells.…”

Section: Introductionmentioning

confidence: 99%

“…The surface layer consists of flat periderm cells, similar to the rest of the oral epithelia, and the basal layer consists of cuboidal ectoderm cells. Soon after palatal shelf elevation, periderm cells covering the medial edge epithelia (MEE) of the palatal shelves bulge from the surface (Fitchett and Hay, 1989;MartinezAlvarez et al, 2000), extend filopodia and lamellipodia (Waterman et al, 1973;Meller et al, 1980;Schupbach et al, 1983;Taya et al, 1999), and undergo programmed cell death (Shapiro and Sweney, 1969;Fitchett and Hay, 1989). Periderm cell death was observed specifically in the MEE before palatal shelves contact each other and was suggested to facilitate adherence of the exposed basal epithelial cells during palatal contact (Waterman et al, 1973;Fitchett andHay, 1989, reviewed in Nawshad et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Jag2‐Notch1 signaling regulates oral epithelial differentiation and palate development

Casey

Lan

Cho

et al. 2006

Developmental Dynamics

122

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During mammalian palatogenesis, palatal shelves initially grow vertically from the medial sides of the paired maxillary processes flanking the developing tongue and subsequently elevate and fuse with each other above the tongue to form the intact secondary palate. Pathological palate-mandible or palate-tongue fusions have been reported in humans and other mammals, but the molecular and cellular mechanisms that prevent such aberrant adhesions during normal palate development are unknown. We previously reported that mice deficient in Jag2, which encodes a cell surface ligand for the Notch family receptors, have cleft palate associated with palate-tongue fusions. In this report, we show that Jag2 is expressed throughout the oral epithelium and is required for Notch1 activation during oral epithelial differentiation. We show that Notch1 is normally highly activated in the differentiating oral periderm cells covering the developing tongue and the lateral oral surfaces of the mandibular and maxillary processes during palate development. Oral periderm activation of Notch1 is significantly attenuated during palate development in the Jag2 mutants. Further molecular and ultrastructural analyses indicate that oral epithelial organization and periderm differentiation are disrupted in the Jag2 mutants. Moreover, we show that the Jag2 mutant tongue fused to wild-type palatal shelves in recombinant explant cultures. These data indicate that Jag2-Notch1 signaling is spatiotemporally regulated in the oral epithelia during palate development to prevent premature palatal shelf adhesion to other oral tissues and to facilitate normal adhesion between the elevated palatal shelves.

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“…In studies of medial edge epithelial (MEE) cell fate during palatal fusion, three different mechanisms have been proposed to account for the disappearance of the MEE from the midline position of the forming secondary palate. First, a long-standing hypothesis proposed that disappearance of MEE cells was a result of classical programmed cell death (Shapiro and Sweney, 1969;Pratt and Martin, 1975;Pratt et al, 1984;Clarke et al, 1993). Second, another hypothesis for the fate of the MEE stated that MEE cells underwent an epithelial-mesenchymal transformation and remained in the connective tissue of the secondary palate as viable mesenchymal cells (Fitchett and Hay, 1989;Griffith and Hay, 1992;Shuler et al, 1991Shuler et al, , 1992Shuler, 1995).…”

Section: Introductionmentioning

confidence: 99%