Mesenchymal cell remodeling during mouse secondary palate reorientation

Jin, Jiu-Zhen; Tan, Min; Warner, Dennis R.; Darling, Douglas S.; Higashi, Youichirou; Gridley, Thomas; Ding, Jixiang

doi:10.1002/dvdy.22339

Cited by 32 publications

(63 citation statements)

References 38 publications

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“…The Zeb1 mutant line has been previously reported by Dr. Yujiro Higashi (Takagi et al, 1998). Further analysis of the palate defects in this mutant were also described by Jin et al, (Jin et al, 2008, Jin et al, 2010. …”

mentioning

confidence: 68%

“…2). In Zeb1 mutant embryos, the two palatal shelves do not contact because of a delay in reorientation (Jin et al, 2008, Jin et al, 2010. However, Mmp13 was still highly expressed in the MEE from anterior end to posterior soft palate indicating that its expression was independent of palatal shelf contact (Fig.…”

Section: Resultsmentioning

confidence: 96%

“…Mmp13 is expressed during mouse palate development, exclusively in MEE cells on E14.5 and E15.5 (Blavier et al, 2001, Jin et al, 2008, Jin et al, 2010. This expression is regulated by TGF-b3 because Mmp13 expression in Tgf-b3 mutant MEE cells is significantly decreased (Blavier et al, 2001).…”

Section: Resultsmentioning

confidence: 99%

“…Since tissue recombination experiments revealed that the MEE cells received signals from the underlying mesenchymal cells, we hypothesized that these mesenchymal cells were also divergent. We determined the expression Goosecoid (Gsc), a marker for the cells underlying the medial edge (Jin et al, 2010, Proetzel et al, 1995 and found that it was present roughly in regions I and II, but not in region III based on the characteristic morphology of posterior soft palate (Fig. 5C), suggesting that the medial edge mesenchymal cells adjacent to the MEE along the A-P axis were indeed different than cells located deeper in the mesenchyme and that this could determine MEE regional specification along A-P axis.…”

Section: Resultsmentioning

confidence: 99%

“…However, Mmp13 was still highly expressed in the MEE from anterior end to posterior soft palate indicating that its expression was independent of palatal shelf contact (Fig. 1E) (Jin et al, 2008, Jin et al, 2010). …”

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confidence: 96%

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Regional divergence of palate medial edge epithelium along the anterior to posterior axis

Jin¹,

Warner²,

Ding³

2014

Int. J. Dev. Biol.

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Recent studies have shown that mouse palatal mesenchymal cells undergo regional specification along the anterior-posterior (A-P) axis defined by anterior Shox2 and Msx1 expression and posterior Meox2 expression. A-P regional specification of the medial edge epithelium, which is directly responsible for palate fusion, has long been proposed, but it has not yet been demonstrated due to the lack of regional specific markers. In this study, we have demonstrated that the palate medial edge epithelium is regionalized along the A-P axis, similar to that for the underlying mesenchyme. Mmp13, a medial edge epithelium specific marker, was uniformly expressed from anterior to posterior in wild-type mouse palatal shelves. Previous studies demonstrated that medial edge epithelium expression of Mmp13 was regulated by TGF-b3. We have found that the changes in Mmp13 expression in TGF-b3 knockouts varied along the A-P axis, and can be broken down into three distinct regions. These regions correlated with regional specification of the underlying medial edge mesenchymal cells and timing of palate fusion. Mouse palate medial edge epithelium along the A-P axis can be divided into different regions according to the differential response to the loss of TGF-b3. KEY WORDS: Mmp13, TGF-b3, mouse secondary palate, regional specificationMammalian palatogenesis is a complex developmental process in which the bilateral palate shelves fuse along the facial midline to form the continuous palate that separates the oral and nasal cavities (Bush and Jiang, 2012, Ferguson, 1988, Murray and Schutte, 2004, Nawshad et al., 2004. Each nascent palatal shelf is made up of a core of neural crest-derived mesenchymal cells enclosed by multiple layers of ectoderm-derived epithelial sheets (Bush and Jiang, 2012, Chai and Maxson, 2006, Ferguson, 1988. In mice, between embryonic day 12.5 and 13.5 (E12.5-E13.5) the two developing palatal shelves first grow in a vertical direction lateral to the tongue. On E14.5, however, the vertical palatal shelves re-orient to form horizontal shelves above the dorsal side of the tongue. The two horizontal palatal shelves continue to grow until they meet each other at their medial edge epithelium (MEE) areas (Bush and Jiang, 2012, Chai and Maxson, 2006, Ferguson, 1988. MEE contact induces a series of cellular events that culminates in the elimination of the epithelial seam formed from the union of the palatal shelves. This medial edge seam (MES) disappears by E15.5 leading to the mesenchymal confluence of the definitive palate (Carette and Ferguson, 1992, Griffith and Hay, 1992, Shuler et al., 1992. MEE cells are critical players in the process of fuInt. J. Dev. Biol. 58: 713-717 (2014) Abbreviations used in this paper: A-P, anterior-posterior; E14.5/15.5, embryonic day 14.5/15.5; MEE, medial edge epithelium; R, rugae; WT, wild type.sion and their differentiation is determined in part by signals from the underlying medial edge mesenchymal cells as demonstrated by tissue recombination experiments (Ferguson et al., 1...

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mentioning

confidence: 68%

Section: Resultsmentioning

confidence: 96%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 96%

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Regional divergence of palate medial edge epithelium along the anterior to posterior axis

Jin¹,

Warner²,

Ding³

2014

Int. J. Dev. Biol.

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Extracellular Matrix in Secondary Palate Development

Logan

Ruest

Benson

et al. 2019

The Anatomical Record

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The secondary palate arises from outgrowths of epithelia-covered embryonic mesenchyme that grow from the maxillary prominence, remodel to meet over the tongue, and fuse at the midline. These events require the coordination of cell proliferation, migration, and gene expression, all of which take place in the context of the extracellular matrix (ECM). Palatal cells generate their ECM, and then stiffen, degrade, or otherwise modify its properties to achieve the required cell movement and organization during palatogenesis. The ECM, in turn, acts on the cells through their matrix receptors to change their gene expression and thus their phenotype. The number of ECM-related gene mutations that cause cleft palate in mice and humans is a testament to the crucial role the matrix plays in palate development and a reminder that understanding that role is vital to our progress in treating palate deformities. This article will review the known ECM constituents at each stage of palatogenesis, the mechanisms of tissue reorganization and cell migration through the palatal ECM, the reciprocal relationship between the ECM and gene expression, and human syndromes with cleft palate that arise from mutations of ECM proteins and their regulators. Anat Rec, 303:1543Rec, 303: -1556Rec, 303: , 2020

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Lithium‐induced overexpression of β‐catenin delays murine palatal shelf elevation by Cdc‐42 mediated F‐actin remodeling in mesenchymal cells

Wang

Liu

et al. 2020

Birth Defects Research

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Background Lithium chloride (LiCl) is widely used for the treatment of manic and other psychotic disorders, but the administration of lithium can result in several congenital defects in the fetus, including cleft palate (Meng, Wang, Torensma, Jw & Bian, 2015) (Szabo, 1970). However, the mechanism of Lithium's action as a developmental toxicant in palatogenesis is not well known. Methods In this study, hematoxylin‐eosin and immunofluorescence staining were employed to evaluate the phenotypes and the expression of related markers in the LiCl‐treated mice model. The palatal mesenchymal cells were cultured in vitro, and stimulated with LiCl or SKL2000, and co‐treated with CASIN. β‐catenin protein and other cytoskeleton associated markers were evaluated by Western blotting. Results We found that Lithium disrupted palate elevation by increasing the expression of β‐catenin in C57BL/6J mice with the high incidence of cleft palate (62.5%). LiCl disturbed the F‐actin responsible for cytoskeletal remodeling in mesenchymal cells, which proved to be essential in generating the elevating force during palatal elevation. Additionally, our Western blotting analysis revealed that the overexpression of β‐catenin resulted in up‐regulation of Cdc42, which mediated the downstream F‐actin synthesis. Conclusions We concluded the LiCl‐induced β‐catenin overexpression delayed murine palatal shelf elevation by disturbing Cdc42 mediated F‐actin cytoskeleton synthesis in the palatal mesenchyme.

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Mesenchymal cell remodeling during mouse secondary palate reorientation

Cited by 32 publications

References 38 publications

Regional divergence of palate medial edge epithelium along the anterior to posterior axis

Regional divergence of palate medial edge epithelium along the anterior to posterior axis

Extracellular Matrix in Secondary Palate Development

Lithium‐induced overexpression of β‐catenin delays murine palatal shelf elevation by Cdc‐42 mediated F‐actin remodeling in mesenchymal cells

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