Palate Development - Revision history

Z8600021 at 00:17, 7 November 2019

2019-11-07T00:17:11Z

← Older revision		Revision as of 10:17, 7 November 2019
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			* '''Short stature homeobox 2 (SHOX2) regulates osteogenic differentiation and pattern formation during hard palate development in mice'''{{#pmid:31649032\|PMID31649032}} "During mammalian palatogenesis, cranial neural crest-derived mesenchymal cells undergo osteogenic differentiation and form the hard palate, which is divided into palatine process of the maxilla and the palatine. However, it remains unknown whether these bony structures originate from the same cell lineage and how the hard palate is patterned at the molecular level. Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. Shox2 overexpression in palatal mesenchyme resulted in a hyperplastic palatine process of the maxilla and a hypoplastic palatine. RNA-Seq and assay for transposase-accessible chromatin (ATAC)-Seq analyses revealed that SHOX2 controls the expression of pattern-specification and skeletogenic genes associated with accessible chromatin in the anterior palate. This highlighted a lineage-autonomous function of SHOX2 in patterning and osteogenesis of the hard palate. H3K27ac ChIP-Seq and transient transgenic enhancer assays revealed that SHOX2 binds distal-acting cis-regulatory elements in an anterior palate-specific manner. Our results suggest that the palatine process of the maxilla and palatine arise from different cell lineages and differ in ossification mechanisms. SHOX2 evidently controls osteogenesis of a cell lineage and contributes to the palatine process of the maxilla by interacting with distal cis-regulatory elements to regulate skeletogenic gene expression and to pattern the hard palate. Genome-wide SHOX2 occupancy in the developing palate may provide a marker for identifying active anterior palate-specific gene enhancers."

	* '''{{TGF-beta}} (TGF-β) Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "Signaling by transforming growth factor {{TGF-beta}} 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. ...{{mouse}} 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."		* '''{{TGF-beta}} (TGF-β) Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "Signaling by transforming growth factor {{TGF-beta}} 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. ...{{mouse}} 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."
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	\| {{Older papers}}		\| {{Older papers}}

	* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893\|PMID23613893}} "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."		* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893\|PMID23613893}} "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."

Z8600021 at 23:29, 12 March 2019

2019-03-12T23:29:48Z

← Older revision		Revision as of 09:29, 13 March 2019
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: ''~~Cleft~~ Palate''		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Palate+Development ''Palate Development''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Palate+Embryology ''Palate Embryology''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Embryonic+Palate ''Embryonic Palate''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Fetal+Palate ''Fetal Palate''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Cleft+Palate ''Cleft Palate''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=levator+veli+palatini+Development levator veli palatini Development]

	~~Search~~ term: ''Palate ~~Embryology~~''

	\|}		\|}

Z8600021 at 23:02, 12 March 2019

2019-03-12T23:02:45Z

← Older revision		Revision as of 09:02, 13 March 2019
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	* '''Ectopic Hedgehog Signaling Causes Cleft Palate and Defective Osteogenesis'''{{#pmid:29975848\|PMID29975848}} "Cleft palate is a common birth defect that frequently occurs in human congenital malformations caused by mutations in components of the Sonic Hedgehog ({{SHH}}) signaling cascade. Shh is expressed in dynamic, spatiotemporal domains within epithelial rugae and plays a key role in driving epithelial-mesenchymal interactions that are central to development of the secondary palate. However, the gene regulatory networks downstream of Hedgehog (Hh) signaling are incompletely characterized. Here, we show that ectopic Hh signaling in the palatal mesenchyme disrupts oral-nasal patterning of the neural crest cell-derived ectomesenchyme of the palatal shelves, leading to defective palatine bone formation and fully penetrant cleft palate. We show that a series of Fox transcription factors, including the novel direct target Foxl1, function downstream of Hh signaling in the secondary palate. Furthermore, we demonstrate that {{Wnt}}/bone morphogenetic protein ({{BMP}}) antagonists, in particular Sostdc1, are positively regulated by Hh signaling, concomitant with down-regulation of key regulators of osteogenesis and BMP signaling effectors."		* '''Ectopic Hedgehog Signaling Causes Cleft Palate and Defective Osteogenesis'''{{#pmid:29975848\|PMID29975848}} "Cleft palate is a common birth defect that frequently occurs in human congenital malformations caused by mutations in components of the Sonic Hedgehog ({{SHH}}) signaling cascade. Shh is expressed in dynamic, spatiotemporal domains within epithelial rugae and plays a key role in driving epithelial-mesenchymal interactions that are central to development of the secondary palate. However, the gene regulatory networks downstream of Hedgehog (Hh) signaling are incompletely characterized. Here, we show that ectopic Hh signaling in the palatal mesenchyme disrupts oral-nasal patterning of the neural crest cell-derived ectomesenchyme of the palatal shelves, leading to defective palatine bone formation and fully penetrant cleft palate. We show that a series of Fox transcription factors, including the novel direct target Foxl1, function downstream of Hh signaling in the secondary palate. Furthermore, we demonstrate that {{Wnt}}/bone morphogenetic protein ({{BMP}}) antagonists, in particular Sostdc1, are positively regulated by Hh signaling, concomitant with down-regulation of key regulators of osteogenesis and BMP signaling effectors."

			* '''Three-dimensional imaging of palatal muscles in the human embryo and fetus: Development of levator veli palatini and clinical importance of the lesser palatine nerve'''{{#pmid:26509917\|PMID26509917}} "The development of LVP in human embryos and fetuses has not been systematically analyzed using the Carnegie stage (CS) to standardize documentation of development. The anlage of LVP starts to develop at CS {{CS21}} beneath the aperture of the auditory tube (AT) to the pharynx. At CS {{CS23}}, LVP runs along AT over its full length, as evidenced by three-dimensional image reconstruction. In the {{fetal}} stage, the lesser palatine nerve (LPN) is in contact with LVP. The positional relationship between LVP and AT three-dimensionally, suggesting that LVP might be derived from the second branchial arch. Based on histological evidence, we hypothesize that motor components from the facial nerve may run along LPN, believed to be purely sensory. The multiple innervation of LVP by LPN and pharyngeal plexus may explain the postpalatoplasty discrepancy between the partial impairment in articulation vs. the functional restoration of deglutition. That is, the contribution of LPN is greater in articulation than in deglutition."

	* '''Molecular Anatomy of Palate Development'''{{#pmid:26168040\|PMID26168040}} "The [https://www.facebase.org NIH FACEBASE] consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. We focused on the {{ME14.5}} palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including both medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate."		* '''Molecular Anatomy of Palate Development'''{{#pmid:26168040\|PMID26168040}} "The [https://www.facebase.org NIH FACEBASE] consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. We focused on the {{ME14.5}} palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including both medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate."
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	Search term: ''Cleft Palate''		Search term: ''Cleft Palate''

	~~<pubmed limit=5>Cleft Palate</pubmed>~~

	Search term: ''Palate Embryology''		Search term: ''Palate Embryology''

	~~<pubmed limit=5>Palate Embryology</pubmed>~~
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"

Z8600021 at 20:50, 23 November 2018

2018-11-23T20:50:18Z

← Older revision		Revision as of 06:50, 24 November 2018
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	{{#pmid:30029495}}		{{#pmid:30029495}}

			{{#pmid:29655165}}

	{{#pmid:26589921}}		{{#pmid:26589921}}

Z8600021 at 20:49, 23 November 2018

2018-11-23T20:49:45Z

← Older revision		Revision as of 06:49, 24 November 2018
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	===Reviews===		===Reviews===
	Indian J Plast Surg. 2009 October; 42(Suppl):[http://www.ncbi.nlm.nih.gov/pmc/issues/185089 Cleft Lip and Palate Issue]		Indian J Plast Surg. 2009 October; 42(Suppl):[http://www.ncbi.nlm.nih.gov/pmc/issues/185089 Cleft Lip and Palate Issue]

			{{#pmid:30463190}}

			{{#pmid:30029495}}

	{{#pmid:26589921}}		{{#pmid:26589921}}

Z8600021 at 20:48, 23 November 2018

2018-11-23T20:48:24Z

← Older revision		Revision as of 06:48, 24 November 2018
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	* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."		* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."

			* '''Ectopic Hedgehog Signaling Causes Cleft Palate and Defective Osteogenesis'''{{#pmid:29975848\|PMID29975848}} "Cleft palate is a common birth defect that frequently occurs in human congenital malformations caused by mutations in components of the Sonic Hedgehog ({{SHH}}) signaling cascade. Shh is expressed in dynamic, spatiotemporal domains within epithelial rugae and plays a key role in driving epithelial-mesenchymal interactions that are central to development of the secondary palate. However, the gene regulatory networks downstream of Hedgehog (Hh) signaling are incompletely characterized. Here, we show that ectopic Hh signaling in the palatal mesenchyme disrupts oral-nasal patterning of the neural crest cell-derived ectomesenchyme of the palatal shelves, leading to defective palatine bone formation and fully penetrant cleft palate. We show that a series of Fox transcription factors, including the novel direct target Foxl1, function downstream of Hh signaling in the secondary palate. Furthermore, we demonstrate that {{Wnt}}/bone morphogenetic protein ({{BMP}}) antagonists, in particular Sostdc1, are positively regulated by Hh signaling, concomitant with down-regulation of key regulators of osteogenesis and BMP signaling effectors."

	* '''Molecular Anatomy of Palate Development'''{{#pmid:26168040\|PMID26168040}} "The [https://www.facebase.org NIH FACEBASE] consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. We focused on the {{ME14.5}} palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including both medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate."		* '''Molecular Anatomy of Palate Development'''{{#pmid:26168040\|PMID26168040}} "The [https://www.facebase.org NIH FACEBASE] consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. We focused on the {{ME14.5}} palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including both medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate."
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	===Articles===		===Articles===
			{{#pmid:29975848}}

			{{#pmid:28296336}}

	{{#pmid:20149609}}		{{#pmid:20149609}}

Z8600021 at 20:42, 23 November 2018

2018-11-23T20:42:31Z

← Older revision		Revision as of 06:42, 24 November 2018
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	* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."		* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."

	* '''~~Regulation~~ of ~~the Epithelial Adhesion Molecule CEACAM1 Is Important for~~ Palate ~~Formation~~'''{{#pmid:~~23613893~~\|~~PMID23613893~~}} "~~Cleft palate results from~~ a ~~mixture~~ of ~~genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse~~. ~~The objective~~ of ~~this study was~~ to ~~search for new genes involved in mouse palate formation. Gene~~ expression of murine ~~embryonic palatal tissue was analyzed at various developmental stages before~~, ~~during, and~~ after ~~palate~~ fusion ~~using GeneChip® microarrays. Ceacam1 was one~~ of the ~~highly up-regulated genes during~~ palate ~~formation~~, and ~~this was confirmed by quantitative real~~-~~time PCR~~. ~~Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium~~ and ~~was degraded during fusion~~. .~~..These~~ results ~~suggest that CEACAM1 has roles in~~ the ~~initiation of palatal fusion via epithelial cell adhesion~~."		* '''Molecular Anatomy of Palate Development'''{{#pmid:26168040\|PMID26168040}} "The [https://www.facebase.org NIH FACEBASE] consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. We focused on the {{ME14.5}} palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including both medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate."

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	\| {{Older papers}}		\| {{Older papers}}
			* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893\|PMID23613893}} "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."

	* '''Role of GSK-3β in the Osteogenic Differentiation of Palatal Mesenchyme'''{{#pmid:22022457\|PMID22022457}} "Here, we identify a critical role for GSK-3β in palatogenesis through its direct regulation of canonical Wnt signaling. These findings shed light on critical developmental pathways involved in palatogenesis and may lead to novel molecular targets to prevent cleft palate formation."		* '''Role of GSK-3β in the Osteogenic Differentiation of Palatal Mesenchyme'''{{#pmid:22022457\|PMID22022457}} "Here, we identify a critical role for GSK-3β in palatogenesis through its direct regulation of canonical Wnt signaling. These findings shed light on critical developmental pathways involved in palatogenesis and may lead to novel molecular targets to prevent cleft palate formation."

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	* '''Prof Virginia Diewert''' - [http://www.dentistry.ubc.ca/AboutUs/FacultyStaffList/detail.asp?user_id=152&from_directory=1 Professor of Orthodontics], University of British Columbia, who recently visited the Lab and helped with content, organisation and development of the [[Palate Development]] section.		* '''Prof Virginia Diewert''' - [http://www.dentistry.ubc.ca/AboutUs/FacultyStaffList/detail.asp?user_id=152&from_directory=1 Professor of Orthodontics], University of British Columbia, who recently visited the Lab and helped with content, organisation and development of the [[Palate Development]] section.
			* [https://www.facebase.org NIH FACEBASE] - Comprehensive craniofacial data and resources.
	* '''Medline Plus''' - [http://www.nlm.nih.gov/medlineplus/cleftlipandpalate.html Cleft Lip and Palate]		* '''Medline Plus''' - [http://www.nlm.nih.gov/medlineplus/cleftlipandpalate.html Cleft Lip and Palate]
	* '''Better Health Channel''' - [http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Cleft_palate_and_cleft_lip Cleft palate and cleft lip]		* '''Better Health Channel''' - [http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Cleft_palate_and_cleft_lip Cleft palate and cleft lip]

Z8600021 at 20:33, 23 November 2018

2018-11-23T20:33:27Z

← Older revision		Revision as of 06:33, 24 November 2018
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	* '''{{TGF-beta}} (TGF-β} Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "Signaling by transforming growth factor {{TGF-beta}} 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. ...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."		* '''{{TGF-beta}} (TGF-β) Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "Signaling by transforming growth factor {{TGF-beta}} 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. ...{{mouse}} 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."

	* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."		* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."

Z8600021 at 20:29, 23 November 2018

2018-11-23T20:29:43Z

← Older revision		Revision as of 06:29, 24 November 2018
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	* '''TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "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. ...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."		* '''{{TGF-beta}} (TGF-β} Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "Signaling by transforming growth factor {{TGF-beta}} 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. ...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."

	* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."		* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."

Z8600021 at 20:27, 23 November 2018

2018-11-23T20:27:11Z

← Older revision		Revision as of 06:27, 24 November 2018
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	* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893\|PMID23613893}} "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."

	* '''~~Role of GSK~~-~~3β in~~ the ~~Osteogenic Differentiation of~~ Palatal ~~Mesenchyme~~'''{{#pmid:~~22022457~~\|~~PMID22022457~~}} "~~Here~~, ~~we identify a critical role for GSK-3β~~ in palatogenesis ~~through its direct regulation~~ of ~~canonical Wnt signaling~~. ~~These findings shed light on critical developmental pathways involved~~ in ~~palatogenesis~~ and ~~may lead~~ to ~~novel molecular targets to prevent cleft palate formation~~."		* '''TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion'''{{#pmid:30463190\|PMID30463190}} "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. ...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."

			* '''Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry'''{{#pmid:30320695\|PMID30320695}} "In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other."

			* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893\|PMID23613893}} "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."

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	\| {{Older papers}}		\| {{Older papers}}
			* '''Role of GSK-3β in the Osteogenic Differentiation of Palatal Mesenchyme'''{{#pmid:22022457\|PMID22022457}} "Here, we identify a critical role for GSK-3β in palatogenesis through its direct regulation of canonical Wnt signaling. These findings shed light on critical developmental pathways involved in palatogenesis and may lead to novel molecular targets to prevent cleft palate formation."

	* '''Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism'''{{#pmid:21246652\|PMID21246652}} "Secondary palate fusion requires adhesion and epithelial-to-mesenchymal transition (EMT) of the epithelial layers on opposing palatal shelves. This EMT requires transforming growth factor β3 (TGFβ3), and its failure results in cleft palate. Ephrins, and their receptors, the Ephs, are responsible for migration, adhesion, and midline closure events throughout development. Ephrins can also act as signal-transducing receptors in these processes, with the Ephs serving as ligands (termed "reverse" signaling). We found that activation of ephrin reverse signaling in chicken palates induced fusion in the absence of TGFβ3, and that PI3K inhibition abrogated this effect. Further, blockage of reverse signaling inhibited TGFβ3-induced fusion in the chicken and natural fusion in the mouse. Thus, ephrin reverse signaling is necessary and sufficient to induce palate fusion independent of TGFβ3."		* '''Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism'''{{#pmid:21246652\|PMID21246652}} "Secondary palate fusion requires adhesion and epithelial-to-mesenchymal transition (EMT) of the epithelial layers on opposing palatal shelves. This EMT requires transforming growth factor β3 (TGFβ3), and its failure results in cleft palate. Ephrins, and their receptors, the Ephs, are responsible for migration, adhesion, and midline closure events throughout development. Ephrins can also act as signal-transducing receptors in these processes, with the Ephs serving as ligands (termed "reverse" signaling). We found that activation of ephrin reverse signaling in chicken palates induced fusion in the absence of TGFβ3, and that PI3K inhibition abrogated this effect. Further, blockage of reverse signaling inhibited TGFβ3-induced fusion in the chicken and natural fusion in the mouse. Thus, ephrin reverse signaling is necessary and sufficient to induce palate fusion independent of TGFβ3."