Aortic Cell Clusters in Vertebrate Embryos

Jordan, H. E.

doi:10.1073/pnas.3.3.149

Cited by 49 publications

(28 citation statements)

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“…However, hematopoietic cell clusters that protrude from the endothelium have been observed not only here, but also in other hemogenic sites, including the vitelline and umbilical arteries, yolk sac, and placenta [23,26,[61][62][63]. Lineage tracing indicates that EHT also occurs in those tissues [27,28,64].…”

Section: Hemogenic Activity -An Inherent Property Of All Young Endothsupporting

confidence: 52%

“…Lineage tracing indicates that EHT also occurs in those tissues [27,28,64]. All this brings to mind the suggestion made 100 years ago, that hemogenic activity is an inherent property of all young, undifferentiated embryonic endothelium [22,23,62]. In this respect, two recent mouse studies give food for thought.…”

Section: Hemogenic Activity -An Inherent Property Of All Young Endothmentioning

confidence: 93%

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A short history of hemogenic endothelium

Swiers

Rode

Azzoni

et al. 2013

Blood Cells, Molecules, and Diseases

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Definitive hematopoietic cells are generated de novo during ontogeny from a specialized subset of endothelium, the so-called hemogenic endothelium. In this review we give a brief overview of the identification of hemogenic endothelium, explore its links with the HSC lineage, and summarize recent insights into the nature of hemogenic endothelium and the microenvironmental and intrinsic regulators contributing to its transition into blood. Ultimately, a better understanding of the processes controlling the transition of endothelium into blood will advance the generation and expansion of hematopoietic stem cells for therapeutic purposes.

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Section: Hemogenic Activity -An Inherent Property Of All Young Endothsupporting

confidence: 52%

Section: Hemogenic Activity -An Inherent Property Of All Young Endothmentioning

confidence: 93%

A short history of hemogenic endothelium

Swiers

Rode

Azzoni

et al. 2013

Blood Cells, Molecules, and Diseases

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“…The initial observations reported by early 20th-century embryologists of the close association between nascent blood precursors and endothelial cells pioneered a fascinating line of research that led to the accumulation of recent findings on haemangioblast and haemogenic endothelium development (Jordan, 1917;Sabin, 1920;Murray, 1932;Huber et al, 2004;Eilken et al, 2009;Lancrin et al, 2009;Bertrand et al, 2010;Boisset et al, 2010;Kissa and Herbomel, 2010). In the present work, we exploited the ES cell-derived blast colony model system to characterise and investigate the role of the transcription factor SOX7 in early embryonic haematopoiesis.…”

Section: Discussionmentioning

confidence: 99%

SOX7 regulates the expression of VE-cadherin in the haemogenic endothelium at the onset of haematopoietic development

et al. 2012

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SUMMARYAt early stages of vertebrate ontogeny, blood and endothelial cells develop from a common mesodermal progenitor, the haemangioblast. Upon haematopoietic commitment, the haemangioblast generates blood precursors through populations of endothelial cells with haemogenic properties. Although several transcription factors have been implicated in haemangioblast differentiation, the precise mechanisms governing cell fate decisions towards the generation of haemogenic endothelium precursors remain largely unknown. Under defined conditions, embryonic stem (ES) cells can be differentiated into haemangioblast-like progenitors that faithfully recapitulate early embryonic haematopoiesis. Here, we made use of mouse ES cells as a model system to understand the role of SOX7, a member of a large family of transcription factors involved in a wide range of developmental processes. During haemangioblast differentiation, SOX7 is expressed in haemogenic endothelium cells and is downregulated in nascent blood precursors. Gain-of-function assays revealed that the enforced expression of Sox7 in haemangioblast-derived blast colonies blocks further differentiation and sustains the expression of endothelial markers. Thus, to explore the transcriptional activity of SOX7, we focused on the endothelial-specific adhesion molecule VE-cadherin. Similar to SOX7, VE-cadherin is expressed in haemogenic endothelium and is downregulated during blood cell formation. We show that SOX7 binds and activates the promoter of VE-cadherin, demonstrating that this gene is a novel downstream transcriptional target of SOX7. Altogether, our findings suggest that SOX7 is involved in the transcriptional regulation of genes expressed in the haemogenic endothelium and provide new clues to decipher the molecular pathways that drive early embryonic haematopoiesis. KEY WORDS: Haemangioblast, Haematopoiesis, Haemogenic endothelium, SOX7, VE-cadherin (cadherin 5), Mouse

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“…We show here that HSCs emerging in both locations are marked by co-expression of the endothelialspecific marker VE-cadherin and the pan-leukocyte antigen CD45. Phenotypic characterisation using CD31, TIE2, FLK1, Ac-LDL receptors, and CD34 markers demonstrated significant similarities between this VEcadherin dorsal aorta (Jordan, 1917;North et al, 1999;Tavian et al, 1996) and the umbilical cord (North et al, 1999) are often interpreted as haematopoietic cells budding off from the endothelial lining. Occasional disruption of the endothelial basal membrane underlying such clusters suggest active involvement of local endothelium (Tavian et al, 1999).…”

Section: Introductionmentioning

confidence: 89%

Progressive divergence of definitive haematopoietic stem cells from the endothelial compartment does not depend on contact with the foetal liver

et al. 2005

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The yolk sac and the para-aortic splanchnopleura/aorta-genital ridges-mesonephros (P-Sp/AGM) region are the main sites of haematopoietic activity in the mouse embryo at the pre-liver stage of development. By day 11.5 of gestation, the AGM region is capable of autonomous initiation and expansion of definitive haematopoietic stem cells (HSCs). By day 12.5, HSC activity in the AGM region is reduced whilst a second wave of HSCs begins to emerge in the yolk sac. We show here that HSCs emerging in both locations are marked by co-expression of the endothelial-specific marker VE-cadherin and the pan-leukocyte antigen CD45. Phenotypic characterisation using CD31, TIE2,FLK1, Ac-LDL receptors, and CD34 markers demonstrated significant similarities between this VE-cadherin+CD45+ `double-positive'population and endothelial cells suggesting a common origin for these cells. The double-positive fraction also expressed the stem cell markers Kit, Sca1 and AA4.1. Long-term transplantation experiments demonstrated that the double-positive population, which constituted less than 0.05% of the day 11.5 AGM region and the day 12.5 yolk sac, is highly enriched for HSCs. In vitro assays showed that this population is also enriched for myeloid progenitors. During foetal liver colonization, circulating HSCs remained within the VE-cadherin+ cell fraction, although their phenotypic similarity with endothelial cells became less prominent. Upon liver colonisation the majority of HSCs downregulated VE-cadherin, expression of which was completely lost in the adult bone marrow. Partial loss of VE-cadherin expression in HSCs can be observed extra hepatically in the advanced AGM region by E12.5. Similarly, the CD34+KIT+ population in the placenta,recently identified as a reservoir of HSCs, partly lose VE-cadherin expression by E12.5. By culturing isolated E11.5 AGM region and E12.5 yolk sac we show that the developmental switch from a `primary'VE-cadherin+CD45+ to a more `advanced'VE-cadherin-CD45+ phenotype does not require contact of HSCs with the liver and is probably a function of developmental time.

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Aortic Cell Clusters in Vertebrate Embryos

Cited by 49 publications

References 1 publication

A short history of hemogenic endothelium

A short history of hemogenic endothelium

SOX7 regulates the expression of VE-cadherin in the haemogenic endothelium at the onset of haematopoietic development

Progressive divergence of definitive haematopoietic stem cells from the endothelial compartment does not depend on contact with the foetal liver

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