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Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin

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Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin. / Martínez-Estrada, Ofelia M; Lettice, Laura A; Essafi, Abdelkader; Guadix, Juan Antonio; Slight, Joan; Velecela, Víctor; Hall, Emma; Reichmann, Judith; Devenney, Paul S; Hohenstein, Peter; Hosen, Naoki; Hill, Robert E; Muñoz-Chapuli, Ramón; Hastie, Nicholas D.

In: Nature Genetics, Vol. 42, No. 1, 01.2010, p. 89-93.

Research output: Contribution to journalArticle

Harvard

Martínez-Estrada, OM, Lettice, LA, Essafi, A, Guadix, JA, Slight, J, Velecela, V, Hall, E, Reichmann, J, Devenney, PS, Hohenstein, P, Hosen, N, Hill, RE, Muñoz-Chapuli, R & Hastie, ND 2010, 'Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin', Nature Genetics, vol. 42, no. 1, pp. 89-93. https://doi.org/10.1038/ng.494

APA

Martínez-Estrada, O. M., Lettice, L. A., Essafi, A., Guadix, J. A., Slight, J., Velecela, V., ... Hastie, N. D. (2010). Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin. Nature Genetics, 42(1), 89-93. https://doi.org/10.1038/ng.494

Vancouver

Martínez-Estrada OM, Lettice LA, Essafi A, Guadix JA, Slight J, Velecela V et al. Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin. Nature Genetics. 2010 Jan;42(1):89-93. https://doi.org/10.1038/ng.494

Author

Martínez-Estrada, Ofelia M ; Lettice, Laura A ; Essafi, Abdelkader ; Guadix, Juan Antonio ; Slight, Joan ; Velecela, Víctor ; Hall, Emma ; Reichmann, Judith ; Devenney, Paul S ; Hohenstein, Peter ; Hosen, Naoki ; Hill, Robert E ; Muñoz-Chapuli, Ramón ; Hastie, Nicholas D. / Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin. In: Nature Genetics. 2010 ; Vol. 42, No. 1. pp. 89-93.

Bibtex

@article{43a9a11d84d84ed5814b98fda93fa25e,
title = "Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin",
abstract = "The epicardial epithelial-mesenchymal transition (EMT) is hypothesized to generate cardiovascular progenitor cells that differentiate into various cell types, including coronary smooth muscle and endothelial cells, perivascular and cardiac interstitial fibroblasts and cardiomyocytes. Here we show that an epicardial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal progenitor cells and their derivatives. We show that Wt1 is essential for repression of the epithelial phenotype in epicardial cells and during embryonic stem cell differentiation through direct transcriptional regulation of the genes encoding Snail (Snai1) and E-cadherin (Cdh1), two of the major mediators of EMT. Some mesodermal lineages do not form in Wt1-null embryoid bodies, but this effect is rescued by the expression of Snai1, underscoring the importance of EMT in generating these differentiated cells. These new insights into the molecular mechanisms regulating cardiovascular progenitor cells and EMT will shed light on the pathogenesis of heart diseases and may help the development of cell-based therapies.",
keywords = "Animals, Cadherins, Cardiovascular System, Cell Differentiation, Cells, Cultured, Embryo, Mammalian, Embryonic Stem Cells, Epithelium, Gene Expression Regulation, Developmental, Gene Knock-In Techniques, Green Fluorescent Proteins, Immunoblotting, Mesoderm, Mice, Mice, Knockout, Pericardium, Reverse Transcriptase Polymerase Chain Reaction, Stem Cells, Transcription Factors, Transcription, Genetic, WT1 Proteins",
author = "Mart{\'i}nez-Estrada, {Ofelia M} and Lettice, {Laura A} and Abdelkader Essafi and Guadix, {Juan Antonio} and Joan Slight and V{\'i}ctor Velecela and Emma Hall and Judith Reichmann and Devenney, {Paul S} and Peter Hohenstein and Naoki Hosen and Hill, {Robert E} and Ram{\'o}n Mu{\~n}oz-Chapuli and Hastie, {Nicholas D}",
year = "2010",
month = "1",
doi = "10.1038/ng.494",
language = "English",
volume = "42",
pages = "89--93",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "Springer Nature",
number = "1",

}

RIS - suitable for import to EndNote

TY - JOUR

T1 - Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin

AU - Martínez-Estrada, Ofelia M

AU - Lettice, Laura A

AU - Essafi, Abdelkader

AU - Guadix, Juan Antonio

AU - Slight, Joan

AU - Velecela, Víctor

AU - Hall, Emma

AU - Reichmann, Judith

AU - Devenney, Paul S

AU - Hohenstein, Peter

AU - Hosen, Naoki

AU - Hill, Robert E

AU - Muñoz-Chapuli, Ramón

AU - Hastie, Nicholas D

PY - 2010/1

Y1 - 2010/1

N2 - The epicardial epithelial-mesenchymal transition (EMT) is hypothesized to generate cardiovascular progenitor cells that differentiate into various cell types, including coronary smooth muscle and endothelial cells, perivascular and cardiac interstitial fibroblasts and cardiomyocytes. Here we show that an epicardial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal progenitor cells and their derivatives. We show that Wt1 is essential for repression of the epithelial phenotype in epicardial cells and during embryonic stem cell differentiation through direct transcriptional regulation of the genes encoding Snail (Snai1) and E-cadherin (Cdh1), two of the major mediators of EMT. Some mesodermal lineages do not form in Wt1-null embryoid bodies, but this effect is rescued by the expression of Snai1, underscoring the importance of EMT in generating these differentiated cells. These new insights into the molecular mechanisms regulating cardiovascular progenitor cells and EMT will shed light on the pathogenesis of heart diseases and may help the development of cell-based therapies.

AB - The epicardial epithelial-mesenchymal transition (EMT) is hypothesized to generate cardiovascular progenitor cells that differentiate into various cell types, including coronary smooth muscle and endothelial cells, perivascular and cardiac interstitial fibroblasts and cardiomyocytes. Here we show that an epicardial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal progenitor cells and their derivatives. We show that Wt1 is essential for repression of the epithelial phenotype in epicardial cells and during embryonic stem cell differentiation through direct transcriptional regulation of the genes encoding Snail (Snai1) and E-cadherin (Cdh1), two of the major mediators of EMT. Some mesodermal lineages do not form in Wt1-null embryoid bodies, but this effect is rescued by the expression of Snai1, underscoring the importance of EMT in generating these differentiated cells. These new insights into the molecular mechanisms regulating cardiovascular progenitor cells and EMT will shed light on the pathogenesis of heart diseases and may help the development of cell-based therapies.

KW - Animals

KW - Cadherins

KW - Cardiovascular System

KW - Cell Differentiation

KW - Cells, Cultured

KW - Embryo, Mammalian

KW - Embryonic Stem Cells

KW - Epithelium

KW - Gene Expression Regulation, Developmental

KW - Gene Knock-In Techniques

KW - Green Fluorescent Proteins

KW - Immunoblotting

KW - Mesoderm

KW - Mice

KW - Mice, Knockout

KW - Pericardium

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Stem Cells

KW - Transcription Factors

KW - Transcription, Genetic

KW - WT1 Proteins

U2 - 10.1038/ng.494

DO - 10.1038/ng.494

M3 - Article

VL - 42

SP - 89

EP - 93

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

IS - 1

ER -