Blood island formation in attached cultures of murine embryonic stem cells

Bautch, Victoria L.; Stanford, William; Rapoport, Rebecca; Russell, Scott D.; Byrum, Robert S.; Futch, Tracy A.

doi:10.1002/(sici)1097-0177(199601)205:1<1::aid-aja1>3.0.co;2-m

Cited by 70 publications

(15 citation statements)

References 47 publications

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“…In embryoid bodies endothelial cells form a vascular network that can be identified by immunostaining with antibodies to endothelial cell markers such as PECAM (CD31) or ICAM‐2. Blood vessel formation in embryoid bodies mimics the development of the embryonic yolk sac vasculature; it occurs through both vasculogenesis and angiogenesis, and is modulated by a variety of growth factors and cytokines including VEGF and TGF‐β1 (Bautch et al, 1996, 2000; Desbaillets et al, 2000; Gualandris et al, 2000b; Feraud et al, 2001; Ng et al, 2004; Mallet et al, 2006). CD31 and ICAM‐2 have different expression patterns during embryoid body differentiation.…”

Section: Resultsmentioning

confidence: 99%

Transforming growth factor‐beta 1 (TGF‐β1) induces angiogenesis through vascular endothelial growth factor (VEGF)‐mediated apoptosis

Ferrari¹,

Cook²,

Terushkin³

et al. 2009

Journal Cellular Physiology

286

156

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VEGF and TGF‐β1 induce angiogenesis but have opposing effects on endothelial cells. VEGF protects endothelial cells from apoptosis; TGF‐β1 induces apoptosis. We have previously shown that VEGF/VEGF receptor‐2 (VEGFR2) signaling mediates TGF‐β1 induction of apoptosis. This finding raised an important question: Does this mechanism stimulate or inhibit angiogenesis? Here we report that VEGF‐mediated apoptosis is required for TGF‐β1 induction of angiogenesis. In vitro the apoptotic effect of TGF‐β1 on endothelial cells is rapid and followed by a long period in which the cells are refractory to apoptosis induction by TGF‐β1. Inhibition of VEGF/VEGFR2 signaling abrogates formation of cord‐like structures by TGF‐β1 with an effect comparable to that of z‐VAD, an apoptosis inhibitor. Similarly, genetic deficiency of VEGF abolishes TGF‐β1 upregulation of endothelial cell differentiation and formation of vascular structures in embryoid bodies. In vivo TGF‐β1 induces endothelial cell apoptosis as rapidly as in vitro. Inhibition of VEGF blocks TGF‐β1 induction of both apoptosis and angiogenesis, an effect similar to that of z‐VAD. Thus, TGF‐β1 induction of angiogenesis requires a rapid and transient apoptotic effect mediated by VEGF/VEGFR2. This novel, unexpected role of VEGF and VEGFR2 indicates VEGF‐mediated apoptosis as a potential target to control angiogenesis. J. Cell. Physiol. 219: 449–458, 2009. © 2009 Wiley‐Liss, Inc.

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Section: Resultsmentioning

confidence: 99%

Transforming growth factor‐beta 1 (TGF‐β1) induces angiogenesis through vascular endothelial growth factor (VEGF)‐mediated apoptosis

Ferrari¹,

Cook²,

Terushkin³

et al. 2009

Journal Cellular Physiology

286

156

View full text Add to dashboard Cite

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“…In addition to developing into all cell lineages and tissues in vivo (except trophoblasts), ES cells can also differentiate into various cell types in vitro and can respond to many physiological and molecular signals [53][54][55][56][57] . The developmental programmes, geneexpression profiles and cell-signalling pathways of in vitro differentiated ES cells approximate certain aspects of early embryonic development, including early organogenesis [58][59][60][61] . Furthermore, ES cells that have differentiated in vitro provide a tool with which to observe and manipulate transient populations of cells that cannot be studied easily in utero, such as haemangioblasts 56 .…”

Section: Sv40 T Antigenmentioning

confidence: 99%

Gene-trap mutagenesis: past, present and beyond

2001

Self Cite

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Although at least 35,000 human genes have been sequenced and mapped, adequate expression or functional information is available for only approximately 15% of them. Gene-trap mutagenesis is a technique that randomly generates loss-of-function mutations and reports the expression of many mouse genes. At present, several large-scale, gene-trap screens are being carried out with various new vectors, which aim to generate a public resource of mutagenized embryonic stem (ES) cells. This resource now includes more than 8,000 mutagenized ES-cell lines, which are freely available, making it an appropriate time to evaluate the recent advances in this area of genomic technology and the technical hurdles it has yet to overcome.

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“…To ensure relevance of DR-ESCs as a model in which to examine vasculogenesis events, we verified that differentiating DR-ESCs give rise to basic vessel structures (Bautch et al, 1996;Doetschman et al, 1985;Marchetti et al, 2002;Yamashita et al, 2000;Yurugi-Kobayashi et al, 2003) within or adjacent to primordial cardiac tissue. This reflects embryonic formation of major blood vessels (Hislop, 2002;Strilic et al, 2009) that occurs through in situ coalescence of ECs, thereby establishing conduits connecting the developing heart with the systemic circulation.…”

Section: Discussionmentioning

confidence: 89%

“…Development of mesoderm-derived hematopoietic, vascular, and cardiac lineages from differentiating ESCs occurs robustly in serum-exposed EBs (Keller, 2005), giving rise to mural cells (D'Souza et al, 2005;Ema et al, 2003), and ECs that reflect initial in vivo differentiation in yolk sac blood islands (Haar and Ackerman, 1971) (Vittet et al, 1996). Although ESCs lack blood flow, ESC-derived ECs form organized yet primitive vessels that lumenize and provide insight into vessel wall and network assemblies that serve as templates for further remodeling (Bautch et al, 1996;Doetschman et al, 1985;Lucitti et al, 2007;Yamashita et al, 2000). While PC origin (Faal et al, 2019) (Trost et al, 2016) (Volz et al, 2015) (Chen et al, 2016) and growth factors that influence differentiation (Armulik et al, 2011) have been described, the mechanisms underlying emergence are still being established.…”

Section: Introductionmentioning

confidence: 99%

Pericytes Directly Communicate with Emerging Endothelial Cells During Vasculogenesis

Payne

Tewari

Dunkenberger

et al. 2020

Preprint

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SummaryPericytes (PCs), cells that extend along capillaries to contribute stability and other critical functions to established vasculature, are attracting attention from various fields involving vascular-related pathologies. Here, we demonstrate primary evidence of PC communication with endothelial cells (ECs) prior to tube coalescence. Observations of apparent PCs during early embryogenesis urged development of a mouse embryonic stem cell line (DR-ESCs), enabling unique dual-reporter investigations into earliest PC-EC interactions. Live imaging of differentiating DR-ESCs corroborated emergence of a PC lineage, which preceded EC differentiation, and further revealed highly dynamic PC-EC interactions during coordinated vessel formation. We show direct PC-EC communication via cell microinjection and dye-transfer, and RNA-seq analysis indicates a PC-EC coupling mechanism via gap junction Connexin43 (Cx43), exclusively up-regulated throughout DR-ESC differentiation. High resolution imaging of embryonic and postnatal mouse vasculature substantiates Cx43 plaques at PC-EC borders. These findings indicate a new role for PCs during vasculogenesis via Cx43-mediated communication with ECs.

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Blood island formation in attached cultures of murine embryonic stem cells

Cited by 70 publications

References 47 publications

Transforming growth factor‐beta 1 (TGF‐β1) induces angiogenesis through vascular endothelial growth factor (VEGF)‐mediated apoptosis

Transforming growth factor‐beta 1 (TGF‐β1) induces angiogenesis through vascular endothelial growth factor (VEGF)‐mediated apoptosis

Gene-trap mutagenesis: past, present and beyond

Pericytes Directly Communicate with Emerging Endothelial Cells During Vasculogenesis

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