Palatal shelf movement during palatogenesis: a fate map of the fetal mouse palate cultured in vitro

Chou, Ming-Jen; Kosazuma, Tsuneo; Takigawa, Toshiya; Yamada, Shigehito; Takahara, Sachiko; Shiota, Kohei

doi:10.1007/s00429-004-0379-0

Cited by 27 publications

(35 citation statements)

References 33 publications

(31 reference statements)

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“…The methods vary in their ability to stimulate palate development and fusion, and the organ culture has significant advantages in this regard (Chou et al, 2004). In the current study, we observed that Dex appeared to stimulate the thickening of the MEE.…”

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

confidence: 58%

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

confidence: 58%

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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“…Thus, comparisons of the mid-palatal region during palatal fusion with the anterior and posterior regions were an important objective of our study. The anterior and posterior regions of the palate have been reported to fuse mainly by tissue remodeling, whereas the mid-palate closes mainly by medial elongation of the shelf [Chou et al, 2004;Okano et al, 2006]. Periostin was present in the mesenchyme with higher levels of expression in the far anterior and posterior region compared with other regions.…”

Section: Discussionmentioning

confidence: 82%

Spatiotemporal Localization of Periostin and Its Potential Role in Epithelial-Mesenchymal Transition during Palatal Fusion

Kitase¹,

Yamashiro²,

Fu³

et al. 2010

Cells Tissues Organs

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The medial epithelial seam (MES) between the palatal shelves degrades during palatal fusion to achieve the confluence of palatal mesenchyme. Cellular mechanisms underlying the degradation of MES have been proposed, such as apoptosis, epithelial-mesenchymal transition (EMT) and migration of medial edge epithelia (MEE). Extracellular matrix components have been shown to play an important role in EMT in many model systems. Periostin (also known as osteoblast-specific factor-2) is a secreted mesenchymal extracellular matrix component that affects the ability of cells to migrate and/or facilitates EMT during both embryonic development and pathologic conditions. In this study, we evaluated the spatiotemporal expression patterns of periostin during mouse palatal fusion by in situ hybridization and immunofluorescence. Periostin mRNA and protein were present in the palatal mesenchyme, the protein being distributed in a fine fibrillar network and in the basement membrane, but absent from the epithelium. During MES degradation, the protein was strongly expressed in the basement membrane underlying the MES and in some select MEE. Confocal microscopic analysis using an EMT marker, twist1, and an epithelial marker, cytokeratin 14, provided evidence that select MEE were undergoing EMT in association with periostin. Moreover, the major extracellular matrix molecules in basement membrane, laminin and collagen type IV were degraded earlier than periostin. The result is that select MEE establish interactions with periostin in the mesenchymal extracellular matrix, and these new cell-matrix interactions may regulate MEE transdifferentiation during palatal fusion.

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“…In some reports regarding the patterned formation of palatal rugae development, morphogenesis, gene expression patterns, and cellular modulations have been examined partially and separately (Peterkova et al 1987;Sakamoto et al 1989;Takanosu et al 2002;Motabagani 2006;Charles et al 2007;Gritli-Linde 2007). Although one previous study has shown the critical movement patterns of palatal shelves by using carbon particle transplantations during in vitro organ cultivation of the palate, the investigation only mentions the palatal fusion mechanism (Chou et al 2004). In addition, cellular events in rugae-forming regions have been studied together with region-specific proliferation and apoptosis patterns in two separate regions designated as the ruga ridge and the inter-rugae (Luke 1984;Amasaki et al 2002Amasaki et al , 2003Takanosu et al 2002).…”

Section: Introductionmentioning

confidence: 96%

Importance of region-specific epithelial rearrangements in mouse rugae development

et al. 2011

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Epithelial appendages on palatal rugae develop during mouse palatogenesis through epithelial thickening and pattern formation. Recently, the patterned formation of nine rugae was observed together with the specific expression patterns of Shh in rodents. However, no crucial evidence was found for a direct association between Shh expression and the distinct structural formation of rugae. In order to reveal possible relationships, we investigated the morphological changes of rugae and expression patterns of Shh directly by in vitro organ culture at embryonic day 13 (E13) for 2 days. To compare and examine the diverse growing aspects of the palate and rugae, we carefully observed the detailed morphogenesis, with cell proliferation of the rugae occurring between E13 and E14.5. After 2 days of cultivation at E13, DiI micro-injections revealed that the middle part of the palate, adjacent to the upper molar-forming region, contributed to the formation of the subsequent structure of rugae by extensive cell rearrangement and proliferation within the epithelium in the preferred anteroposterior direction. The results also defined the intimate relationship between Shh expression and rugae formation.

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Palatal shelf movement during palatogenesis: a fate map of the fetal mouse palate cultured in vitro

Cited by 27 publications

References 33 publications

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

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

Spatiotemporal Localization of Periostin and Its Potential Role in Epithelial-Mesenchymal Transition during Palatal Fusion

Importance of region-specific epithelial rearrangements in mouse rugae development

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