Aortic arch malformations and ventricular septal defect in mice deficient in endothelin-1.

Kurihara, Yukiko; Kurihara, Hiroki; Oda, Hideaki; Maemura, Koji; Nagai, Ryozo; Ishikawa, Takatoshi; Yazaki, Yoshio

doi:10.1172/jci118033

Cited by 372 publications

(218 citation statements)

References 38 publications

Supporting

Mentioning

209

Contrasting

Order By: Relevance

“…Factors different from ET3, therefore, are likely to control self-renewal and differentiation of myofibroblastic NC precursors. Several candidate signaling molecules are platelet-derived growth factors (44,45), ET1 (46)(47)(48)(49), or members of the TGF␤͞BMPs family (18,(50)(51)(52), which were shown to influence the development of NCC into vascular smooth-muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Self-renewal capacity is a widespread property of various types of neural crest precursor cells

Trentin

Glavieux-Pardanaud²,

Douarin³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

158

179

View full text Add to dashboard Cite

In vertebrates, trunk neural crest (NC) generates glia, neurons, and melanocytes. In addition, it yields mesectodermal derivatives (connective tissues, chondrocytes, and myofibroblasts lining the blood vessels) in the head. Previous in vitro clonal analyses of avian NC cells unraveled a hierarchical succession of highly pluripotent, followed by various intermediate, progenitors, suggesting a model of progressive restrictions in the multiple potentialities of a totipotent stem cell, as prevails in the hematopoietic system. However, which progenitors are able to self-renew within the hierarchy of the NC lineages is still undetermined. Here, we explored further the stem cell properties of quail NC cells by means of in vitro serial subcloning. We identified types of multipotent and oligopotent NC progenitors that differ in their developmental repertoire, ability to self-maintain, and response to exogenous endothelin 3 according to their truncal or cephalic origin. The most striking result is that bipotent progenitors are endowed with self-renewal properties. Thus glia-melanocyte and glia-myofibroblast progenitors behave like stem cells in that they are able both to self-renew and generate a restricted progeny. In our culture conditions, glia-myofibroblast precursors display a modest capacity to self-renew, whereas glia-melanocyte precursors respond to endothelin 3 by extensive self-renewal. These findings may explain the etiology of certain multiphenotypic NC-derived tumors in humans. Moreover, the presence of multiple stem cell phenotypes along the NC-derived lineages may account for the rarity of the ''totipotent NC stem cell'' and may be related to the large variety and widespread dispersion of NC derivatives throughout the body. multipotency ͉ quail embryo ͉ clonal culture ͉ neuron ͉ glia T he neural crest (NC) is a transient structure of the vertebrate embryo formed by the lateral borders of the neural primordium. Its constitutive cells, after losing their epithelial arrangement, migrate away through embryonic tissues to stop at elected sites where they differentiate into many various cell types. These cell types include neurons of the peripheral and enteric ganglia, their associated glial cells, and Schwann cells lining peripheral nerves. The NC is also at the origin of melanocytes and endocrine cells, such as adrenomedullary cells and calcitoninproducing cells. The NC cephalic domain yields mesenchymal cells (forming the ''mesectoderm'') that differentiate into the cartilages and bones that form most of the skull and the entire facial and visceral skeleton. The mesectoderm also provides head connective-tissue cells and the vascular smooth-muscle cells associated with the vessels derived from the aortic arches and with the vessels irrigating the forebrain and face (1-3).Several attempts aimed at elucidating how and when the different NC-lineages become segregated during ontogeny were made by using in vitro cultures of single NC cells (NCC) (4-14) or by labeling single NCC with vital dyes either in the embryo (...

show abstract

Section: Discussionmentioning

confidence: 99%

Self-renewal capacity is a widespread property of various types of neural crest precursor cells

Trentin

Glavieux-Pardanaud²,

Douarin³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

158

179

View full text Add to dashboard Cite

show abstract

“…Instead, we find that Vezf1/DB1 trans-activates ET-1, which appears later than KDR/flk-1 during vascular development. Deficiency of ET-1 during development results in branchial arch abnormalities, leading to defects in branchial arch artery development and subsequent malformation of the great vessels and cardiac outflow tract abnormalities, as well as characteristic craniofacial abnormalities (4,5). If the effects of Vezf1/DB1 on ET-1 expression observed in the present studies are representative of regulatory events that are critical in endothelial cells during vascular development, then absence of Vezf1/DB1 in mice should phenocopy, at least partially, ET-1-null mice.…”

Section: Discussionmentioning

confidence: 99%

“…ET-1, which is expressed primarily in endothelial cells and also epithelial cells of the branchial arches during development (4), is required for the development of neural crest-derived tissues arising from the branchial arches, such as the great vessels, the ventricular septum, and craniofacial structures (5). These effects seem to be mediated via interactions with the endothelin-A receptor, which is expressed in neural crest cells.…”

mentioning

confidence: 99%

Vezf1/DB1 Is an Endothelial Cell-specific Transcription Factor That Regulates Expression of the Endothelin-1 Promoter

Aitsebaomo¹,

Kingsley-Kallesen²,

Wu³

et al. 2001

Journal of Biological Chemistry

View full text Add to dashboard Cite

Coordinated gene regulation within the vascular endothelium is required for normal cardiovascular patterning during development and for vascular homeostasis during adulthood, yet little is known about the mechanisms that regulate endothelial transcriptional events. Vascular endothelial zinc finger 1 (Vezf1)/DB1 is a recently identified zinc finger-containing protein that is expressed specifically within endothelial cells during development. In this report, we demonstrate that Vezf1/ DB1 is a nuclear localizing protein that potently and specifically activates transcription mediated by the human endothelin-1 promoter, in a Tax-independent manner, in transient transfection assays. Using a combination of deletion mutagenesis and electrophoretic mobility shift assays, a novel Vezf1/DB1-responsive element was localized to a 6-base pair (bp) motif, ACCCCC, located 47 bp upstream of the endothelin-1 transcription start site. Recombinant Vezf1/DB1 also bound to this sequence, and a 2-bp mutation in this element abolished Vezf1/DB1 responsiveness by the endothelin-1 promoter. Vezf1/DB1 could be identified with a specific antibody in nuclear complexes from endothelial cells that bound to this element. Regulation of endothelin-1 promoter activity by Vezf1/DB1 provides a mechanism for endothelin-1 expression in the vascular endothelium during development and to maintain vascular tone; Vezf1/DB1 itself is a candidate transcription factor for modifying endothelial cell phenotypes in order to appropriately assemble and maintain the cardiovascular system.

show abstract

“…Furthermore, the Cx43-null mutant phenotype, characterized by infundibular bulging without septation defects, differs from other murine genetic models that affect CNC function. Genetic models including those with mutations in or knockouts of Pax3, neurotrophin 3/TrkC, TGF␤ receptor type II, BMP4, BMP receptor IA, endothelin 1 and combinations of retinoic acid receptors (Choudhary et al, 2006;Donovan et al, 1996;Epstein et al, 2000;Kurihara et al, 1995;Liu et al, 2004;Mendelsohn et al, 1994;Stottmann et al, 2004;Youn et al, 2003) commonly cause OFT septation defects similar to those resulting from chick NC ablation. Thus, during development, Cx43 may be required in tissues that contribute to heart formation other than or in addition to the CNC (Li et al, 2002;Walker et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Distinct cardiac malformations caused by absence of connexin 43 in the neural crest and in the non-crest neural tube

Liu

Schneider

et al. 2006

Development

View full text Add to dashboard Cite

Connexin 43 (Cx43) is expressed in the embryonic heart, cardiac neural crest (CNC) and neural tube, and germline knockout (KO) of Cx43 results in aberrant cardiac outflow tract (OFT) formation and abnormal coronary deployment. Prior studies suggest a vital role for CNC expression of Cx43 in heart development. Surprisingly, we found that conditional knockout (CKO) of Cx43 in the dorsal neural tube and CNC mediated by Wnt1-Cre failed to recapitulate the Cx43-null OFT phenotype, although coronary vasculature was abnormal in this mutant line. A broader CKO mediated by P3pro (Pax3)-Cre, involving both ventral and dorsal aspects of the thoracic neural tube and CNC, resulted in infundibular bulging and coronary anomalies similar to those seen in germline Cx43-null hearts. P3pro-Cre-mediated loss of Cx43 in the neural tube was characterized by a late phase of cellular delamination from the dorsal and lateral neural tube, a markedly increased abundance of neuroepithelium-derived cells outside of the neural tube and an excess of such cells infiltrating the heart and infundibulum. Thus, expression of Cx43 in the CNC is crucial for normal coronary deployment, but Cx43 is not required in the CNC for normal OFT morphogenesis. Rather, this study suggests a novel function for Cx43 in which Cx43 acts through non-crest neuroepithelial cells to suppress cellular delamination from the neural tube and thereby preserve normal OFT development.

show abstract

Aortic arch malformations and ventricular septal defect in mice deficient in endothelin-1.

Cited by 372 publications

References 38 publications

Self-renewal capacity is a widespread property of various types of neural crest precursor cells

Self-renewal capacity is a widespread property of various types of neural crest precursor cells

Vezf1/DB1 Is an Endothelial Cell-specific Transcription Factor That Regulates Expression of the Endothelin-1 Promoter

Distinct cardiac malformations caused by absence of connexin 43 in the neural crest and in the non-crest neural tube

Contact Info

Product

Resources

About