Matrix Metalloproteinases have a Role in Palatogenesis

Brown, Nathan; Yarram, S. J.; Mansell, Jason P.; Sandy, JR

doi:10.1177/154405910208101206

Cited by 55 publications

(59 citation statements)

References 15 publications

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“…Blocking basal lamina degradation by inhibiting MMP activity, however, had no effect on cell death. These results contrast with two recent reports (Blavier et al, 2001;Brown et al, 2002) showing partial or no MEE degeneration in the presence of the same MMP inhibitor used here. In our experiments, we demonstrated [with high reproducibility even at the low inhibitor dose (10 µM)] that the basal lamina was intact.…”

Section: Discussioncontrasting

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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Section: Discussioncontrasting

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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“…In MMP9 analysis, we noted differences for maxillary tooth agenesis but not for mandible tooth agenesis. One possible reason for the difference between the arches may be that MMPs have a role in palatogenesis, and disruption of its activity can result in cleft palate (30). In some instances, oral clefts and tooth agenesis may share the same genetic background (2,31).…”

Section: Discussionmentioning

confidence: 99%

Genetic variations in MMP9 and MMP13 contribute to tooth agenesis in a Brazilian population

et al. 2013

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We investigated the association between polymorphisms in the MMP2 (rs243865), MMP9 (rs17576), and MMP13 (rs2252070) genes with tooth agenesis in humans. Two hundred eighty-five unrelated individuals (202 controls without tooth agenesis and 83 cases with tooth agenesis) were evaluated in a cross-sectional single-center study. The study participants were recruited through the Pediatric Dental Clinics of the Federal University of Rio de Janeiro, Brazil. Genotyping of the selected polymorphisms for MMPs was carried out by real-time PCR using the Taqman assay method from genomic DNA isolated from buccal epithelial cells of all the studied individuals. There was no significant association of MMP2 genotype or allele distribution with tooth agenesis or its absence. For MMP9, a significant difference in allele frequency was evident between the two groups (P = 0.05). With regard to the affected side, there was a significant difference between unilateral tooth agenesis and the control group in the distribution of MMP9 (P = 0.05). Also, there was a significant difference in MMP9 distribution between tooth agenesis in the maxilla and control individuals (P = 0.03). The genotype distribution of MMP13 differed significantly between the group with unilateral tooth agenesis and the controls (P = 0.01). Our findings provide evidence that MMP9 and MMP13 may be involved in tooth agenesis. (J Oral Sci 55, 281-286, 2013)

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“…In the case of palatal MEE cells, the cells seem to develop greater matrix-dependency for survival and become sensitive to anoikis during EMT, because EMT is always associated with integrin-mediated cell scattering on the substrates, defined by the loss of intercellular junctions and acquisition of cell motility (Hay, 1995;Boyer et al, 2000). Recently, Blavier et al (2001) and Brown et al (2002) showed that the activity of MMPs (matrix metalloproteinases) is indispensable for disappearance of the MEE seam and disruption of its basement membrane during palatal fusion, and that at least MT1-MMP, MMP-13, and MMP-3 are expressed in the MEE at the time of midline seam disruption. These MMPs are known to digest not only type IV collagen and laminins of basement membrane but also a variety of other extracellular matrix components, such as fibronectin, type I and III collagens, and proteoglycans (Werb, 1997;Seiki, 2003).…”

Section: G D E H F I Jmentioning

confidence: 99%

“…Although palate organ cultures enable various experiments which are impossible in utero, they sometimes produce conflicting results. Palate culture methods reported thus far can be largely divided into the static culture method using a CO 2 incubator (Pourtois, 1966(Pourtois, , 1968Smiley and Koch, 1971, 1972, 1975Dixon and Ferguson, 1992;Griffith and Hay, 1992;Martínez-Álvarez et al, 2000;Cuervo et al, 2002;Cuervo and Covarrubias, 2004) and the suspension culture method with rolling bottles (Shiota et al, 1990;Brown et al, 2002). In those cultures, some fundamental questions remain such as: (1) In order from the left, oral and medial views of the single shelf explants, and the cell morphology of the medial edge and oral and nasal epithelia, respectively.…”

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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Matrix Metalloproteinases have a Role in Palatogenesis

Cited by 55 publications

References 15 publications

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

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

Genetic variations in MMP9 and MMP13 contribute to tooth agenesis in a Brazilian population

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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