Developmental Mechanism - Epithelial Mesenchymal Transition - Revision history

Z8600021 at 23:48, 12 September 2020

2020-09-12T23:48:31Z

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	{{#pmid:31277295}}		{{#pmid:31277295}}

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	{{#pmid:12894994}}		{{#pmid:12894994}}

	===Articles===		===Articles===

Z8600021 at 23:47, 12 September 2020

2020-09-12T23:47:17Z

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			* '''Sox9 promotes renal tubular epithelial‑mesenchymal transition and extracellular matrix aggregation via the PI3K/AKT signaling pathway'''{{#pmid:32901875\|PMID32901875}} "Sox9 is important for multiple aspects of development, such as testis, pancreas and heart development. Previous studies have reported that Sox9 induced epithelial‑mesenchymal transition (EMT) and extracellular matrix (ECM) production in organ fibrosis and associated diseases, such as vascular calcification. However, to the best of our knowledge, the role and underlying mechanism of action of Sox9 in renal fibrogenesis remains unknown. The results of the present study revealed that Sox9 expression levels were upregulated in the tubular epithelial cells of a rat model of obstructive nephropathy. Furthermore, the overexpression of Sox9 in NRK‑52E cells was discovered to promote renal tubular EMT and ECM aggregation, and these fibrogenic actions were potentiated by TGF‑β1. Notably, RNA‑sequencing analysis indicated the possible regulatory role of the PI3K/AKT signaling pathway in Sox9‑mediated renal tubular EMT and ECM aggregation. It was further demonstrated that the expression levels of phosphorylated AKT were upregulated in NRK‑52E cells overexpressing Sox9, while the PI3K inhibitors, LY29002 and wortmannin, inhibited the renal tubular EMT and ECM aggregation induced by the overexpression of Sox9 in NEK‑52E cells. In conclusion, the findings of the present study suggested that Sox9 may serve a profibrotic role in the development of renal tubular EMT and ECM aggregation via the PI3K/AKT signaling pathway. Therefore, Sox9 may be considered as a promising target for treating renal fibrosis."

	* '''p120-catenin regulates {{WNT}} signaling and EMT in the mouse embryo.'''{{#pmid:31371508\|PMID31371508}} "{{epithelial mesenchymal transition}}s (EMTs) require a complete reorganization of cadherin-based cell-cell junctions. p120-catenin binds to the cytoplasmic juxtamembrane domain of classical cadherins and regulates their stability, suggesting that p120-catenin may play an important role in EMTs. Here, we describe the role of p120-catenin in {{mouse}} {{gastrulation}}, an EMT that can be imaged at cellular resolution and is accessible to genetic manipulation. Mouse embryos that lack all p120-catenin, or that lack p120-catenin in the embryo proper, survive to midgestation. However, mutants have specific defects in gastrulation, including a high rate of p53-dependent cell death, a bifurcation of the posterior axis, and defects in the migration of mesoderm; all are associated with abnormalities in the primitive streak, the site of the EMT. In embryonic day 7.5 (E7.5) mutants, the domain of expression of the streak marker Brachyury (T) expands more than 3-fold, from a narrow strip of posterior cells to encompass more than one-quarter of the embryo. After {{ME7.5}}, the enlarged T+ domain splits in 2, separated by a mass of {{mesoderm}} cells. Brachyury is a direct target of canonical WNT signaling, and the domain of {{WNT}} response in p120-catenin mutant embryos, like the T domain, is first expanded, and then split, and high levels of nuclear β-catenin levels are present in the cells of the posterior embryo that are exposed to high levels of WNT ligand. The data suggest that p120-catenin stabilizes the membrane association of β-catenin, thereby preventing accumulation of nuclear β-catenin and excessive activation of the WNT pathway during EMT."		* '''p120-catenin regulates {{WNT}} signaling and EMT in the mouse embryo.'''{{#pmid:31371508\|PMID31371508}} "{{epithelial mesenchymal transition}}s (EMTs) require a complete reorganization of cadherin-based cell-cell junctions. p120-catenin binds to the cytoplasmic juxtamembrane domain of classical cadherins and regulates their stability, suggesting that p120-catenin may play an important role in EMTs. Here, we describe the role of p120-catenin in {{mouse}} {{gastrulation}}, an EMT that can be imaged at cellular resolution and is accessible to genetic manipulation. Mouse embryos that lack all p120-catenin, or that lack p120-catenin in the embryo proper, survive to midgestation. However, mutants have specific defects in gastrulation, including a high rate of p53-dependent cell death, a bifurcation of the posterior axis, and defects in the migration of mesoderm; all are associated with abnormalities in the primitive streak, the site of the EMT. In embryonic day 7.5 (E7.5) mutants, the domain of expression of the streak marker Brachyury (T) expands more than 3-fold, from a narrow strip of posterior cells to encompass more than one-quarter of the embryo. After {{ME7.5}}, the enlarged T+ domain splits in 2, separated by a mass of {{mesoderm}} cells. Brachyury is a direct target of canonical WNT signaling, and the domain of {{WNT}} response in p120-catenin mutant embryos, like the T domain, is first expanded, and then split, and high levels of nuclear β-catenin levels are present in the cells of the posterior embryo that are exposed to high levels of WNT ligand. The data suggest that p120-catenin stabilizes the membrane association of β-catenin, thereby preventing accumulation of nuclear β-catenin and excessive activation of the WNT pathway during EMT."

	* '''Self-organization of a human organizer by combined Wnt and Nodal signalling'''{{#pmid:29795348\|PMID29795348}} "In amniotes, the development of the primitive streak and its accompanying 'organizer' define the first stages of gastrulation. Although these structures have been characterized in detail in model organisms, the human primitive streak and organizer remain a mystery. When stimulated with {{BMP}}4, micropatterned colonies of human embryonic stem cells self-organize to generate early embryonic germ layers 1 . Here we show that, in the same type of colonies, Wnt signalling is sufficient to induce a primitive streak, and stimulation with Wnt and Activin is sufficient to induce an organizer, as characterized by embryo-like sharp boundary formation, markers of {{epithelial mesenchymal transition}} and expression of the organizer-specific transcription factor GSC. Moreover, when grafted into chick embryos, human stem cell colonies treated with Wnt and Activin induce and contribute autonomously to a secondary axis while inducing a neural fate in the host."
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	\| {{Older papers}}		\| {{Older papers}}
			* '''Self-organization of a human organizer by combined Wnt and Nodal signalling'''{{#pmid:29795348\|PMID29795348}} "In amniotes, the development of the primitive streak and its accompanying 'organizer' define the first stages of gastrulation. Although these structures have been characterized in detail in model organisms, the human primitive streak and organizer remain a mystery. When stimulated with {{BMP}}4, micropatterned colonies of human embryonic stem cells self-organize to generate early embryonic germ layers 1 . Here we show that, in the same type of colonies, Wnt signalling is sufficient to induce a primitive streak, and stimulation with Wnt and Activin is sufficient to induce an organizer, as characterized by embryo-like sharp boundary formation, markers of {{epithelial mesenchymal transition}} and expression of the organizer-specific transcription factor GSC. Moreover, when grafted into chick embryos, human stem cell colonies treated with Wnt and Activin induce and contribute autonomously to a secondary axis while inducing a neural fate in the host."

	* '''p53 coordinates cranial {{neural crest}} cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."		* '''p53 coordinates cranial {{neural crest}} cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."
	\|}		\|}

Z8600021 at 23:43, 12 September 2020

2020-09-12T23:43:22Z

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	Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation. For example, within the mesoderm {{somite}} epithelium, the sclerotome component undergoes EMT forming the skeletal elements of the vertebrae and ribs. Other examples occur in neural crest formation, heart valve formation and Müllerian duct regression.		Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation. For example, within the mesoderm {{somite}} epithelium, the sclerotome component undergoes EMT forming the skeletal elements of the vertebrae and ribs. Other examples occur in neural crest formation, heart valve formation and Müllerian duct regression.

			<center>'''''Mechanism''' - "a process, technique, or system for achieving a result".''</center>

	~~<center>'''''Mechanism''' - "a process, technique, or system for achieving a result".''</center>~~

	This process is also studied in carcinogenesis (oncogenesis) or cancer development, where part of this process can be the transformation of an epithelial cell into a mesenchymal cell.{{#pmid:20943648\|PMID20943648}}{{#pmid:21559368\|PMID21559368}}		This process is also studied in carcinogenesis (oncogenesis) or cancer development, where part of this process can be the transformation of an epithelial cell into a mesenchymal cell.{{#pmid:20943648\|PMID20943648}}{{#pmid:21559368\|PMID21559368}}
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Epithelial+Mesenchymal+Transition ''Epithelial Mesenchymal Transition'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Epithelial+Mesenchymal+Transition ''Epithelial Mesenchymal Transition''] \|
			[http://www.ncbi.nlm.nih.gov/pubmed/?term=TWIST ''TWIST''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=ZEB ''ZEB''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=SNAIL ''SNAIL'']
	\|}		\|}
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	\| {{Older papers}}		\| {{Older papers}}
	* '''p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."		* '''p53 coordinates cranial {{neural crest}} cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."
	\|}		\|}
	==Cell Junction Changes==		==Cell Junction Changes==

Z8600021 at 01:35, 23 April 2020

2020-04-23T01:35:45Z

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	===Search PubMed===		===Search PubMed===


	'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Epithelial+Mesenchymal+Transition Epithelial Mesenchymal Transition]		'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Epithelial+Mesenchymal+Transition Epithelial Mesenchymal Transition]

	==External Links==		==External Links==

	{{External Links}}		{{External Links}}

			* EMT International Association [https://temtia.org TEMTIA]

	----		----

	{{Mechanism Links}}		{{Mechanism Links}}


	{{Glossary}}		{{Glossary}}


	{{Footer}}		{{Footer}}

	[[Category:Developmental Mechanism]]		[[Category:Developmental Mechanism]]

Z8600021 at 01:32, 23 April 2020

2020-04-23T01:32:46Z

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	:'''Links:''' {{gastrulation}}		:'''Links:''' {{gastrulation}}

			==Somite Development==
			The paraxial mesoderm segments to form {{somite}}s The sclerotome component of each somite undergoes EMT grating away and eventually forming the axial skeletal elements of the {{vertebrae}} and {{rib}}s.


			{{Somite cartoon}}

			:'''Links:''' {{somite}}

	==Neural Crest Development==		==Neural Crest Development==

Z8600021 at 01:27, 23 April 2020

2020-04-23T01:27:31Z

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	Epithelial cells (organised cellular layer) which loose their organisation and migrate/proliferate as a mesenchymal cells (disorganised cellular layers) are said to have undergone an Epithelial Mesenchymal Transition (EMT).		Epithelial cells (organised cellular layer) which loose their organisation and migrate/proliferate as a mesenchymal cells (disorganised cellular layers) are said to have undergone an Epithelial Mesenchymal Transition (EMT).

	Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation ~~for~~ example in neural crest formation, heart valve formation and Müllerian duct regression.		Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation. For example, within the mesoderm {{somite}} epithelium, the sclerotome component undergoes EMT forming the skeletal elements of the vertebrae and ribs. Other examples occur in neural crest formation, heart valve formation and Müllerian duct regression.


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	* '''p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."		* '''p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes'''{{#pmid:21447558\|PMID21447558}} "Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects."
	\|}		\|}
			==Cell Junction Changes==

			Epithelial cells are connected by many different cell junctions, that mesenchymamal cells either lack or redistribute. Epithelial cell junctions include adherens junctions, desmosomes, gap junctions and tight junctions.

			Mesenchymal cells interact with extracellular matrix and establish polarity in actin stress fibres and intermediate filament focal adhesions.

			'''Epithelial or Mesenchymal Cell State'''{{#pmid:32300252\|PMID32300252}}

			[[File:Epithelial Mesenchymal Transition.jpg\|800px]]


	==Gastrulation==		==Gastrulation==

Z8600021 at 01:07, 23 April 2020

2020-04-23T01:07:17Z

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	Epithelial cells (organised cellular layer) which loose their organisation and migrate/proliferate as a mesenchymal cells (disorganised cellular layers) are said to have undergone an Epithelial Mesenchymal Transition (EMT).		Epithelial cells (organised cellular layer) which loose their organisation and migrate/proliferate as a mesenchymal cells (disorganised cellular layers) are said to have undergone an Epithelial Mesenchymal Transition (EMT).

	Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation.		Mesenchymal cells, connective tissue-like, that have undergone this process may at a later time and under specific signaling can undergo the opposite process, mesenchyme to epithelia. In development, this process can be repeated several times during tissue differentiation for example in neural crest formation, heart valve formation and Müllerian duct regression.


			<center>'''''Mechanism''' - "a process, technique, or system for achieving a result".''</center>

	~~<center>'''''Mechanism''' - "a~~ process, ~~technique, or system for achieving~~ a ~~result"~~.~~''</center>~~		This process is also studied in carcinogenesis (oncogenesis) or cancer development, where part of this process can be the transformation of an epithelial cell into a mesenchymal cell.{{#pmid:20943648\|PMID20943648}}{{#pmid:21559368\|PMID21559368}}


	~~This process is also~~ studied in ~~carcinogenesis (oncogenesis) or cancer development, where part of this process can be the transformation of an epithelial cell into a mesenchymal cell~~.{{#pmid:~~20943648\|PMID20943648}}{{#pmid:21559368~~\|~~PMID21559368~~}}		Historically, in the late 1970s Elizabeth Hay began studied “epithelial–mesenchymal transformation” in embryogenesis.{{#pmid:8714286\|PMID8714286}}

Z8600021 at 00:59, 23 April 2020

2020-04-23T00:59:17Z

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	==Neural Crest Development==		==Neural Crest Development==

	Early neural crest cell development migration involves an initial {{epithelial mesenchymal transition}} to delaminate from the {{ectoderm}} layer.{{#pmid:30476447\|PMID30476447}})		Early {{neural crest}} cell development migration involves an initial {{epithelial mesenchymal transition}} to delaminate from the {{ectoderm}} neural tube layer.{{#pmid:30476447\|PMID30476447}} A microRNA miR-203, acting as part of an epigenetic-microRNA regulatory network, appears influence the timing of this neural crest delamination.{{#pmid:30910825\|PMID30910825}}


	:'''Links:''' {{neural crest}}		:'''Links:''' {{neural crest}}
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	===Reviews===		===Reviews===
			{{#pmid:32048783}}

			{{#pmid:32300252}}

			{{#pmid:31277295}}

			{{#pmid:12894994}}
	===Articles===		===Articles===

			{{#pmid:32234315}}

			{{#pmid:31371508}}

			{{#pmid:30910825}}

	===Search PubMed===		===Search PubMed===

Z8600021 at 00:47, 23 April 2020

2020-04-23T00:47:44Z

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	The Zinc Finger E Box-Binding Homeobox (ZEB) family of 2-handed zinc finger/homeodomain proteins and functions as a DNA-binding transcriptional repressor that interacts with activated SMADs, the transducers of {{TGF-beta}} signaling.		The Zinc Finger E Box-Binding Homeobox (ZEB) family of 2-handed zinc finger/homeodomain proteins and functions as a DNA-binding transcriptional repressor that interacts with activated SMADs, the transducers of {{TGF-beta}} signaling.

			Expression of ZEB1 in human epithelial cells can cause a morphologic change from an epithelial to a mesenchymal phenotype.{{#pmid:16314317\|}PMID16314317}}


			:'''Links:''' [https://www.omim.org/entry/189909 ZEB1] \| [https://www.omim.org/entry/605802 ZEB2]

	==Mesenchymal-to-Epithelial Transition==		==Mesenchymal-to-Epithelial Transition==

Z8600021 at 00:41, 23 April 2020

2020-04-23T00:41:14Z

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	:'''Links:''' [[Endocrine_-_Other_Tissues#Endocrine_Lung\|Endocrine Respiratory]] \| {{Respiratory}}		:'''Links:''' [[Endocrine_-_Other_Tissues#Endocrine_Lung\|Endocrine Respiratory]] \| {{Respiratory}}

			==Molecular==
			TWIST, ZEB, SNAIL

			===Twist===
			The twist family (TWIST1, TWIST2) of basic helix-loop-helix transcription factors are expressed in embryonic mesoderm and have been shown to be key regulators of the epithelial-mesenchymal transition. These transcription factors recognize a consensus DNA element called the E box. Mouse and human TWIST share 96.6% amino acid identity.


			:'''Links:''' [https://www.omim.org/entry/601622 TWIST1] \| [https://www.omim.org/entry/607556 TWIST2]

			===ZEB===

			The Zinc Finger E Box-Binding Homeobox (ZEB) family of 2-handed zinc finger/homeodomain proteins and functions as a DNA-binding transcriptional repressor that interacts with activated SMADs, the transducers of {{TGF-beta}} signaling.

	==Mesenchymal-to-Epithelial Transition==		==Mesenchymal-to-Epithelial Transition==