scholarly journals Medial Edge Epithelial Cell Fate during Palatal Fusion

2000 ◽  
Vol 220 (2) ◽  
pp. 343-357 ◽  
Author(s):  
C. Martı́nez-Álvarez ◽  
C. Tudela ◽  
J. Pérez-Miguelsanz ◽  
S. O'Kane ◽  
J. Puerta ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Palatal Fusion ◽  
Medial Edge

scholarly journals Constitutive activation of hedgehog signaling adversely affects epithelial cell fate during palatal fusion

2018 ◽  
Vol 441 (1) ◽  
pp. 191-203 ◽  
Author(s):  
Jingyuan Li ◽  
Yuan Yuan ◽  
Jinzhi He ◽  
Jifan Feng ◽  
Xia Han ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Hedgehog Signaling ◽  
Constitutive Activation ◽  
Palatal Fusion

The fate of medial edge epithelial cells during palatal fusion in vitro: an analysis by DiI labelling and confocal microscopy

Development ◽  
1992 ◽  
Vol 114 (2) ◽  
pp. 379-388 ◽  
Author(s):  
M.J. Carette ◽  
M.W. Ferguson
Keyword(s):  
Laser Scanning ◽  
Time Course ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Palatal Fusion ◽  
Morphological Criteria ◽  
Medial Edge ◽  
Mesenchymal Transformation

Fusion of bilateral shelves, to form the definitive mammalian secondary palate, is critically dependent on removal of the medial edge cells that constitute the midline epithelial seam. Conflicting views suggest that programmed apoptotic death or epithelial-mesenchymal transformation of these cells is predominantly involved. Due in part to the potentially ambiguous interpretation of static images and the notable absence of fate mapping studies, the process by which this is achieved has, however, remained mechanistically equivocal. Using an in vitro mouse model, we have selectively labelled palatal epithelia with DiI and examined the fate of medial edge epithelial (MEE) cells during palatal fusion by localisation using a combination of conventional histology and confocal laser scanning microscopy (CLSM). In dynamic studies using CLSM, we have made repetitive observations of the same palatal cultures in time-course investigations. Our results concurred with the established morphological criteria of seam degeneration; however, they provided no evidence of MEE cell death or transformation. Instead we report that MEE cells migrate nasally and orally out of the seam and are recruited into, and constitute, epithelial triangles on both the oral and nasal aspects of the palate. Subsequently these cells become incorporated into the oral and nasal epithelia on the surface of the palate. We hypothesize an alternative method of seam degeneration in vivo which largely conserves the MEE population by recruiting it into the nasal and oral epithelia.

scholarly journals TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion

2018 ◽  
Vol 19 (11) ◽  
pp. 3638 ◽  
Author(s):  
Akira Nakajima ◽  
Charles F. Shuler ◽  
Alexander Gulka ◽  
Jun-ichi Hanai
Keyword(s):  
Cell Fate ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Genetically Engineered ◽  
Fusion Process ◽  
Mesenchymal Transition ◽  
Morphological Process ◽  
Palatal Fusion ◽  
Genetically Engineered Mice

Signaling by transforming growth factor (TGF)-β plays an important role in development, including in palatogenesis. The dynamic morphological process of palatal fusion occurs to achieve separation of the nasal and oral cavities. Critically and specifically important in palatal fusion are the medial edge epithelial (MEE) cells, which are initially present at the palatal midline seam and over the course of the palate fusion process are lost from the seam, due to cell migration, epithelial-mesenchymal transition (EMT), and/or programed cell death. In order to define the role of TGF-β signaling during this process, several approaches have been utilized, including a small interfering RNA (siRNA) strategy targeting TGF-β receptors in an organ culture context, the use of genetically engineered mice, such as Wnt1-cre/R26R double transgenic mice, and a cell fate tracing through utilization of cell lineage markers. These approaches have permitted investigators to distinguish some specific traits of well-defined cell populations throughout the palatogenic events. In this paper, we summarize the current understanding on the role of TGF-β signaling, and specifically its association with MEE cell fate during palatal fusion. TGF-β is highly regulated both temporally and spatially, with TGF-β3 and Smad2 being the preferentially expressed signaling molecules in the critical cells of the fusion processes. Interestingly, the accessory receptor, TGF-β type 3 receptor, is also critical for palatal fusion, with evidence for its significance provided by Cre-lox systems and siRNA approaches. This suggests the high demand of ligand for this fine-tuned signaling process. We discuss the new insights in the fate of MEE cells in the midline epithelial seam (MES) during the palate fusion process, with a particular focus on the role of TGF-β signaling.

scholarly journals Apc deficiency alters pulmonary epithelial cell fate and inhibits Nkx2.1 via triggering TGF-beta signaling

2013 ◽  
Vol 378 (1) ◽  
pp. 13-24 ◽  
Author(s):  
Changgong Li ◽  
Aimin Li ◽  
Yiming Xing ◽  
Min Li ◽  
Belinda Chan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Tgf Beta ◽  
Pulmonary Epithelial Cell

scholarly journals Autophagy Is a Component of Epithelial Cell Fate in Obstructive Uropathy

2010 ◽  
Vol 176 (4) ◽  
pp. 1767-1778 ◽  
Author(s):  
Ling Li ◽  
Diana Zepeda-Orozco ◽  
Rachel Black ◽  
Fangming Lin
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Obstructive Uropathy

p21WAF1 Control of Epithelial Cell Cycle and Cell Fate

2002 ◽  
Vol 13 (6) ◽  
pp. 453-464 ◽  
Author(s):  
Wendy C. Weinberg ◽  
Mitchell F. Denning
Keyword(s):  
Cell Cycle ◽  
Epithelial Cell ◽  
Cell Fate ◽  
Cell Biology ◽  
Kinase Inhibitor ◽  
Growth Arrest ◽  
Nuclear Antigen ◽  
Central Position ◽  
Cyclin Dependent Kinase ◽  
Cyclin Dependent Kinase Inhibitor

As a broad-acting cyclin-dependent kinase inhibitor, p21WAF1 occupies a central position in the cell cycle regulation of self-renewing tissues such as oral mucosa and skin. In addition to regulating normal cell cycle progression decisions, p21WAF1 integrates genotoxic insults into growth arrest and apoptotic signaling pathways that ultimately determine cell fate. As a result of its complex interactions with cell cycle machinery and response to mutagenic agents, p21WAF1 also has stage-specific roles in epithelial carcinogenesis. Finally, a view is emerging of p21WAF1 as not merely a cyclin-dependent kinase inhibitor, but also as a direct participant in regulating genes involved in growth arrest, senescence, and aging, thus providing an additional layer of control over matters of the cell cycle. This review discusses these various roles played by p21WAF1 in cell cycle control, and attempts to relate these to epithelial cell biology, with special emphasis on keratinocytes. (Abbreviations used include the following: Brdu, 5-Bromo-2-deoxyuridine; cdk, cyclin-dependent kinase; EGF, epidermal growth factor; KIP, kinase inhibitor protein; PCNA, proliferating cell nuclear antigen; and TPA, 12-O-tetradecanoylphorbol-13-acetate.)

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