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Paul A. Krieg - One of the best experts on this subject based on the ideXlab platform.
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Hedgehog signaling is essential for endothelial tube formation during vasculogenesis.
Development (Cambridge England), 2004Co-Authors: Steven A. Vokes, Tatiana A. Yatskievych, Ronald L. Heimark, Jill A. Mcmahon, Andrew P. Mcmahon, Parker B. Antin, Paul A. KriegAbstract:During embryonic development, the first blood vessels are formed through the aggregation and subsequent assembly of Angioblasts (endothelial precursors) into a network of endothelial tubes, a process known as vasculogenesis. These first vessels generally form in mesoderm that is adjacent to endodermal tissue. Although specification of the Angioblast lineage is independent of endoderm interactions, a signal from the endoderm is necessary for Angioblasts to assemble into a vascular network and to undergo vascular tube formation. In this study, we show that endodermally derived sonic hedgehog is both necessary and sufficient for vascular tube formation in avian embryos. We also show that Hedgehog signaling is required for vascular tube formation in mouse embryos, and for vascular cord formation in cultured mouse endothelial cells. These results demonstrate a previously uncharacterized role for Hedgehog signaling in vascular development, and identify Hedgehog signaling as an important component of the molecular pathway leading to vascular tube formation.
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Endoderm is required for vascular endothelial tube formation, but not for Angioblast specification.
Development (Cambridge England), 2002Co-Authors: Steven A. Vokes, Paul A. KriegAbstract:Angioblasts, the precursor cells that comprise the endothelial layer of blood vessels, arise from a purely mesodermal population. Individual Angioblasts coalesce to form the primary vascular plexus through a process called vasculogenesis. A number of reports in the literature suggest that signals from the adjacent endoderm are necessary to induce Angioblast specification within the mesoderm. We present evidence, using both embryological and molecular techniques, indicating that endoderm is not necessary for the induction of Angioblasts. Xenopus embryos that had endoderm physically removed at the onset of gastrulation still express vascular markers. Furthermore, animal caps stimulated with bFGF form Angioblasts in the absence of any detectable endodermal markers. These results show that endoderm is not required for the initial formation of Angioblasts. While Xenopus embryos lacking endoderm contain aggregates of Angioblasts, these Angioblasts fail to assemble into endothelial tubes. Endothelial tube formation can be rescued, however, by implantation of endodermal tissue from sibling embryos. Based on these studies in Xenopus, and corroborating experiments using the quail embryo, we conclude that endoderm is not required for Angioblast specification, but does play an essential role in the formation of vascular tubes.
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vegf mediates Angioblast migration during development of the dorsal aorta in xenopus
Development, 1998Co-Authors: Ondine Cleaver, Paul A. KriegAbstract:Angioblasts are precursor cells of the vascular endothelium which organize into the primitive blood vessels during embryogenesis. The molecular mechanisms underlying patterning of the embryonic vasculature remain unclear. Mutational analyses of the receptor tyrosine kinase flk-1 and its ligand vascular endothelial growth factor, VEGF, indicate that these molecules are critical for vascular development. Targeted ablation of the flk-1 gene results in complete failure of blood and vascular development (F. Shalaby et al. (1995) Nature 376, 62–66), while targeted ablation of the VEGF gene results in gross abnormalities in vascular patterning (P. Carmeliet et al. (1996) Nature 380, 435–439; N. Ferrara et al. (1996) Nature 380, 439–442). Here we report a role for VEGF in patterning the dorsal aorta of the Xenopus embryo. We show that the diffusible form of VEGF is expressed by the hypochord, which lies at the embryonic midline immediately dorsal to the location of the future dorsal aorta. We find that, initially, no flk-1-expressing Angioblasts are present at this location, but that during subsequent development, Angioblasts migrate from the lateral plate mesoderm to the midline where they form a single dorsal aorta. We have demonstrated that VEGF can act as a chemoattractant for Angioblasts by ectopic expression of VEGF in the embryo. These results strongly suggest that localized sources of VEGF play a role in patterning the embryonic vasculature.
Werner Risau - One of the best experts on this subject based on the ideXlab platform.
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identification of vascular endothelial growth factor vegf receptor 2 flk 1 promoter enhancer sequences sufficient for Angioblast and endothelial cell specific transcription in transgenic mice
Blood, 1999Co-Authors: Andreas Kappel, Werner Risau, Annette Damert, Ingo Flamme, Volker Ronicke, Georg BreierAbstract:The vascular endothelial growth factor (VEGF) receptor-2 (Flk-1) is the first endothelial receptor tyrosine kinase to be expressed in Angioblast precursors, and its function is essential for the differentiation of endothelial cells and hematopoietic precursors. We have identified cis-acting regulatory elements of the murine Flk-1 gene that mediate endothelium-specific expression of a LacZ reporter gene in transgenic mice. Sequences within the 5'-flanking region of the Flk-1 gene, in combination with sequences located in the first intron, specifically targeted transgene expression to Angioblasts and endothelial cells of transgenic mice. The intronic regulatory sequences functioned as an autonomous endothelium-specific enhancer. Sequences of the 5'-flanking region contributed to a strong, uniform, and reproducible transgene expression and were stimulated by the transcription factor HIF-2alpha. The Flk-1 gene regulatory elements described in this study should allow the elucidation of the molecular mechanisms involved in endothelial cell differentiation and angiogenesis.
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Identification of Vascular Endothelial Growth Factor (VEGF) Receptor-2 (Flk-1) Promoter/Enhancer Sequences Sufficient for Angioblast and Endothelial Cell-Specific Transcription in Transgenic Mice
Blood, 1999Co-Authors: Andreas Kappel, Werner Risau, Volker Rönicke, Annette Damert, Ingo Flamme, Georg BreierAbstract:The vascular endothelial growth factor (VEGF) receptor-2 (Flk-1) is the first endothelial receptor tyrosine kinase to be expressed in Angioblast precursors, and its function is essential for the differentiation of endothelial cells and hematopoietic precursors. We have identified cis-acting regulatory elements of the murineFlk-1 gene that mediate endothelium-specific expression of a LacZ reporter gene in transgenic mice. Sequences within the 5′-flanking region of the Flk-1 gene, in combination with sequences located in the first intron, specifically targeted transgene expression to Angioblasts and endothelial cells of transgenic mice. The intronic regulatory sequences functioned as an autonomous endothelium-specific enhancer. Sequences of the 5′-flanking region contributed to a strong, uniform, and reproducible transgene expression and were stimulated by the transcription factor HIF-2. The Flk-1 gene regulatory elements described in this study should allow the elucidation of the molecular mechanisms involved in endothelial cell differentiation and angiogenesis.
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Embryonic angiogenesis factors
Pharmacology & therapeutics, 1991Co-Authors: Werner RisauAbstract:The vascular system develops during embryonic development by at least two distinct processes; vasculogenesis is the development of blood vessels from in situ differentiating Angioblasts and angiogenesis is the sprouting of capillaries from pre-existing vessels. The molecular mechanisms involved in the regulation of these processes are poorly understood. Endoderm-mesoderm interactions seem to play an important role in Angioblast differentiation and vasculogenesis. Soluble angiogenic factors may be involved in the vascularization of some embryonic organs, e.g. kidney and brain. Angiogenic growth factors have been isolated and purified from embryonic brain and identified as acidic and basic fibroblast growth factors. More specific endothelial cell growth factors such as platelet-derived endothelial cell growth factor and vascular endothelial growth factor may also play a role in embryonic angiogenesis.
Shuo Lin - One of the best experts on this subject based on the ideXlab platform.
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Molecular Medicine Etsrp/Etv2 Is Directly Regulated by Foxc1a/b in the
2016Co-Authors: Zebrafish Angioblast, Matthew B. Veldman, Shuo LinAbstract:Rationale: Endothelial cells are developmentally derived from Angioblasts specified in the mesodermal germ cell layer. The transcription factor etsrp/etv2 is at the top of the known genetic hierarchy for Angioblast development. The transcriptional events that induce etsrp expression and Angioblast specification are not well understood. Objective: We generated etsrp:gfp transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for etsrp expression and Angioblast specification from mesoderm. Methods and Results: To investigate the mechanisms that initiate Angioblast cell transcription during embryo-genesis, we have performed promoter analysis of the etsrp locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all 3 regulatory regions led to a near complete loss of endothelial expression from the etsrp promoter. One of the enhancers, located 2.3 kb upstream of etsrp contains a consensus FOX binding site that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP. Combined knockdown of foxc1a/b, using morpholinos, led to a significant decrease in etsrp expression at early developmental stages as measured by quantitative reverse transcriptase–polymerase chain reaction and in situ hybridization. Decreased expression of primitive erythrocyte genes scl and gata1 was also observed, whereas pronephric gene pax2a was relatively normal in expression level and pattern. Conclusions: These findings identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in Angioblasts. This establishes a new molecular link in the process of mesoderm specification into Angioblast. (Circ Res. 2012
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Etsrp/Etv2 Is Directly Regulated by Foxc1a/b in the
2016Co-Authors: Zebrafish Angioblast, Matthew B. Veldman, Shuo LinAbstract:Rationale: Endothelial cells are developmentally derived from Angioblasts specified in the mesodermal germ cell layer. The transcription factor etsrp/etv2 is at the top of the known genetic hierarchy for Angioblast development. The transcriptional events that induce etsrp expression and Angioblast specification are not well understood. Objective: We generated etsrp:gfp transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for etsrp expression and Angioblast specification from mesoderm. Methods and Results: To investigate the mechanisms that initiate Angioblast cell transcription during embryo-genesis, we have performed promoter analysis of the etsrp locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all 3 regulatory regions led to a near complete loss of endothelial expression from the etsrp promoter. One of the enhancers, located 2.3 kb upstream of etsrp contains a consensus FOX binding site that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP. Combined knockdown of foxc1a/b, using morpholinos, led to a significant decrease in etsrp expression at early developmental stages as measured by quantitative reverse transcriptase–polymerase chain reaction and in situ hybridization. Decreased expression of primitive erythrocyte genes scl and gata1 was also observed, whereas pronephric gene pax2a was relatively normal in expression level and pattern. Conclusions: These findings identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in Angioblasts. This establishes a new molecular link in the process of mesoderm specification into Angioblast. (Circ Res. 2012
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Ets1-Related Protein Is a Key Regulator of Vasculogenesis in Zebrafish
2013Co-Authors: Saulius Sumanas, Shuo LinAbstract:During embryonic development, multiple signaling pathways control specification, migration, and differentiation of the vascular endothelial cell precursors, Angioblasts. No single gene responsible for the commitment of mesenchymal cells to the Angioblast cell fate has been identified as yet. Here we report characterization and functional studies of Etsrp, a novel zebrafish ETS domain protein. etsrp embryonic expression is only restricted to vascular endothelial cells and their earliest precursors. Morpholino knockdown of Etsrp protein function resulted in the complete absence of circulation in zebrafish embryos. Angioblasts in etsrp–morpholino-injected embryos (morphants) failed to undergo migration and differentiation and did not coalesce into functional blood vessels. Expression of all vascular endothelial molecular markers tested was severely reduced in etsrp morphants, whereas hematopoietic markers were not affected. Overexpression of etsrp RNA caused multiple cell types to express vascular endothelial markers. etsrp RNA restored expression of vascular markers in cloche mutants, defective in hematopoietic and endothelial cell formation, arguing that etsrp functions downstream of cloche in Angioblast formation. etsrp gene function was also required for endothelial marker induction by the vascular endothelial growth factor (vegf) and stem cell leukemia (scl/tal1). These results demonstrate that Etsrp is necessary and sufficient for the initiation of vasculogenesis. Citation: Sumanas S, Lin S (2006) Ets1-related protein is a key regulator of vasculogenesis in zebrafish. PLoS Biol 4(1): e10
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Molecular Analysis of Early Vasculogenesis in etsrp Morphants
2013Co-Authors: Saulius Sumanas, Shuo LinAbstract:(A, B, E, F, I, K) Uninjected control embryo; (C, D, G, H, J, L) 8–10 ng etsrp MO2-injected embryo. Anterior is to the left in all panels. (A–H) Embryos were flat mounted with their yolk removed. (A–D) scl expression; six-somite (A,C) and ten-somite (B,D) stages. Note that the anterior domain of scl expression (arrows) is reduced and the trunk domain (arrowheads) is missing in etsrp morphants. (E–H) fli1 expression; six-somite (E,G) and ten-somite (F,H) stages. Note that the anterior domain of fli1 expression (arrows) is missing in the etsrp morphants, while the posterior domain is not affected. Also note that the trunk domain of fli1 expression (arrowheads, F,H) is missing at the ten-somite stage in etsrp morphants. (I–L) Etsrp knockdown blocks Angioblast migration towards the midline as assayed by etsrp expression at the 16-somite (I,J) and 20-somite (K,L) stages. (I,K) Uninjected control embryo; (J,L) 7.5 ng etsrp MO2-injected embryo. Dorsal view, anterior is to the left. Note that the midline stripe of Angioblasts (arrows) is missing in etsrp morphants. Also notice more intense etsrp expression in pre-migratory Angioblasts (arrowheads) in etsrp morphants as compared to control embryos.
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etsrp etv2 is directly regulated by foxc1a b in the zebrafish Angioblast
Circulation Research, 2012Co-Authors: Matthew B. Veldman, Shuo LinAbstract:Rationale:Endothelial cells are developmentally derived from Angioblasts specified in the mesodermal germ cell layer. The transcription factor etsrp/etv2 is at the top of the known genetic hierarchy for Angioblast development. The transcriptional events that induce etsrp expression and Angioblast specification are not well understood. Objective:We generated etsrp:gfp transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for etsrp expression and Angioblast specification from mesoderm. Methods and Results:To investigate the mechanisms that initiate Angioblast cell transcription during embryogenesis, we have performed promoter analysis of the etsrp locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all 3 regulatory regions led to a near complete loss of endothelial expression from the etsrp promoter. One of the enhancers, located 2.3 kb upstream of ets...
Miguel A. Herrero - One of the best experts on this subject based on the ideXlab platform.
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early embryonic vascular patterning by matrix mediated paracrine signalling a mathematical model study
PLOS ONE, 2011Co-Authors: Alvaro Kohnluque, Walter De Back, Andrea Mattiotti, Jorn Starrus, Jose M Perezpomares, Andreas Deutsch, Miguel A. HerreroAbstract:During embryonic vasculogenesis, endothelial precursor cells of mesodermal origin known as Angioblasts assemble into a characteristic network pattern. Although a considerable amount of markers and signals involved in this process have been identified, the mechanisms underlying the coalescence of Angioblasts into this reticular pattern remain unclear. Various recent studies hypothesize that autocrine regulation of the chemoattractant vascular endothelial growth factor (VEGF) is responsible for the formation of vascular networks in vitro. However, the autocrine regulation hypothesis does not fit well with reported data on in vivo early vascular development. In this study, we propose a mathematical model based on the alternative assumption that endodermal VEGF signalling activity, having a paracrine effect on adjacent Angioblasts, is mediated by its binding to the extracellular matrix (ECM). Detailed morphometric analysis of simulated networks and images obtained from in vivo quail embryos reveals the model mimics the vascular patterns with high accuracy. These results show that paracrine signalling can result in the formation of fine-grained cellular networks when mediated by Angioblast-produced ECM. This lends additional support to the theory that patterning during early vascular development in the vertebrate embryo is regulated by paracrine signalling.
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early embryonic vascular patterning by matrix mediated paracrine signalling a mathematical model study
PLOS ONE, 2011Co-Authors: Alvaro Kohnluque, Walter De Back, Andrea Mattiotti, Jorn Starrus, Jose M Perezpomares, Andreas Deutsch, Miguel A. HerreroAbstract:During embryonic vasculogenesis, endothelial precursor cells of mesodermal origin known as Angioblasts assemble into a characteristic network pattern. Although a considerable amount of markers and signals involved in this process have been identified, the mechanisms underlying the coalescence of Angioblasts into this reticular pattern remain unclear. Various recent studies hypothesize that autocrine regulation of the chemoattractant vascular endothelial growth factor (VEGF) is responsible for the formation of vascular networks in vitro. However, the autocrine regulation hypothesis does not fit well with reported data on in vivo early vascular development. In this study, we propose a mathematical model based on the alternative assumption that endodermal VEGF signalling activity, having a paracrine effect on adjacent Angioblasts, is mediated by its binding to the extracellular matrix (ECM). Detailed morphometric analysis of simulated networks and images obtained from in vivo quail embryos reveals the model mimics the vascular patterns with high accuracy. These results show that paracrine signalling can result in the formation of fine-grained cellular networks when mediated by Angioblast-produced ECM. This lends additional support to the theory that patterning during early vascular development in the vertebrate embryo is regulated by paracrine signalling.
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Early Embryonic Vascular Patterning by Matrix-Mediated Paracrine Signalling: A Mathematical Model Study
2011Co-Authors: Walter De Back, Andrea Mattiotti, Andreas Deutsch, Miguel A. HerreroAbstract:During embryonic vasculogenesis, endothelial precursor cells of mesodermal origin known as Angioblasts assemble into a characteristic network pattern. Although a considerable amount of markers and signals involved in this process have been identified, the mechanisms underlying the coalescence of Angioblasts into this reticular pattern remain unclear. Various recent studies hypothesize that autocrine regulation of the chemoattractant vascular endothelial growth factor (VEGF) is responsible for the formation of vascular networks in vitro. However, the autocrine regulation hypothesis does not fit well with reported data on in vivo early vascular development. In this study, we propose a mathematical model based on the alternative assumption that endodermal VEGF signalling activity, having a paracrine effect on adjacent Angioblasts, is mediated by its binding to the extracellular matrix (ECM). Detailed morphometric analysis of simulated networks and images obtained from in vivo quail embryos reveals the model mimics the vascular patterns with high accuracy. These results show that paracrine signalling can result in the formation of fine-grained cellular networks when mediated by Angioblast-produced ECM. This lends additional support to the theory that patterning during early vascular development i
Thomas J. Poole - One of the best experts on this subject based on the ideXlab platform.
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The role of FGF and VEGF in Angioblast induction and migration during vascular development.
Developmental dynamics : an official publication of the American Association of Anatomists, 2001Co-Authors: Thomas J. Poole, Eric B. Finkelstein, Christopher M. CoxAbstract:The embryonic vasculature forms by the processes of vasculogenesis and angiogenesis. Angioblasts (endothelial cell precursors) appear to be induced by fibroblast growth factor 2 (FGF-2). The Angioblasts contributing to the dorsal aortae arise by an epithelial to mesenchymal transformation of cells originating from the splanchnic mesoderm. QH-l and vascular endothelial growth factor receptor 2 (VEGFR-2) both appear to label these cells as they adopt a mesenchymal morphology. Since VEGFR-2 is the earliest known VEGF receptor this suggests that VEGF is not involved in Angioblast induction. VEGF does appear to be critical, however, for growth and morphogenesis of Angioblasts into the initial vascular pattern. Controlled delivery of FGF-2 from beads and aggregates of cells transfected with quail VEGF have been used in our laboratory to study the role of these growth factors in Angioblast induction and migration. We have induced cells from the epithelial quail somite to differentiate into Angioblasts with FGF-2 both in the embryo and in culture. This is a useful model system to study the origins of endothelial cells that are normally more diffusely induced during gastrulation by an obscure process probably involving signals from the embryonic endoderm. The origins of arterial versus venous endothelial cells is also poorly understood but recent findings on the distribution of ephrins and Eph receptors suggest that molecular differences exist prior to the onset of circulation. Finally, studies on the role of growth factors in such diverse phenomena as stem cell biology, angiogenesis, and molecular medicine in addition to vascular development suggest multiple roles for FGF-2 and VEGF in vascular development.
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Angioblast differentiation is influenced by the local environment: FGF-2 induces Angioblasts and patterns vessel formation in the quail embryo
Developmental dynamics : an official publication of the American Association of Anatomists, 2000Co-Authors: Christopher M. Cox, Thomas J. PooleAbstract:The embryonic vasculature forms by the segregation, migration, and assembly of Angioblasts from mesoderm, a process termed vasculogenesis. The initial role of fibroblast growth factor 2 (FGF-2) in vascular development appears to be in the induction of endothelial precursors, Angioblasts. Quail somites transplanted into chick embryos will give rise to Angioblasts of quail origin. The number of Angioblasts present within the chimera is dependent on the host environment. Angioblast induction can be demonstrated in vitro by the addition of FGF-2 to cultures of dissociated somitic mesoderm, as assessed by QH-1 epitope expression. Manipulation of FGF-2 concentration in the quail/chick chimeras by FGF-2 peptide or neutralizing antibody injections increases or decreases Angioblast induction in the predicted manner. To better control growth factor release in vivo we have implanted beads that release FGF-2 into the embryonic environment. FGF-2 beads implanted into the somite induce Angioblast differentiation in the epithelial somite; whereas, beads lateral to the somitic mesoderm induce the formation of ectopic vessels. These studies suggest that FGF-2 is important for both the induction of Angioblasts and the assembly of Angioblasts into the initial vasculature pattern. Dev Dyn;218:371–382. © 2000 Wiley-Liss, Inc.
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Cellular and Molecular Biology of Endothelial Cell Differentiation during Embryonic Development
Angiogenesis, 1994Co-Authors: Thomas J. PooleAbstract:How does the pattern of the rudiments of the major blood vessels establish itself in the developing embryo? To understand the cellular biology of these events we must know how the Angioblasts, the precursors of endothelial cells, segregate from the mesoderm, migrate, and cohere to one another to form the cords and tubes which are the earliest embryonic blood vessels. We have been using a monoclonal antibody (QH-1) and microsurgery to determine where Angioblasts originate and how they assemble into vessel rudiments (Coffin and Poole, 1988; Poole and Coffin, 1989; 1991). The extent and type of directed Angioblast migration define three distinct modes of vessel morphogenesis (Poole and Coffin, 1991; Poole, 1993). Vessel rudiments may organize in place, a process termed vasculogenesis, either from Angioblasts originating at the rudiment’s location (vasculogenesis type I) or from Angioblasts which migrate as individual cells or small groups to that site from different locations (vasculogenesis type II). The dorsal aortae form by the first type of vasculogenesis (Coffin and Poole, 1988; DeRuiter et al., 1993; Pardanaud et al., 1987; Poole and Coffin, 1988; 1989; 1991). The endocardium, ventral aortae and posterior cardinal veins form by the second type (Coffin and Poole, 1991; DeRuiter et al., 1993; Drake and Jacobson, 1988; Poole and Coffin, 1991). New vessels may also form by sprouting from preexisting vessels, a process called angiogenesis. The intersomitic and vertebral arteries are the first vessels to form by angiogenesis, sprouting off the rudiments of the dorsal aortae (Coffin and Poole, 1988; Poole and Coffin, 1988; 1989; 1991). Figure 1 illustrates the different roles of endothelial cells in vasculogenesis and angiogenesis.
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Directed Cell Migration in Embryonic Blood Vessel Assembly
Homing Mechanisms and Cellular Targeting, 1994Co-Authors: Thomas J. PooleAbstract:Publisher Summary Recent advances in the study of endothelial cell origin and assembly were made possible by the production of monoclonal antibodies that labeled Angioblasts and endothelium. Another useful property of these monoclonal antibodies is that they label quail Angioblasts but not chick cells so that endothelial cell differentiation and migration in quail/chick chimeras can be followed. Descriptive studies of quail embryos using the QH-1 antibody revealed that Angioblasts arise at discrete locations and then assemble into cords at the sites of the blood vessel rudiments. These antibodies have also been used at older stages of embryogenesis in parallel with corrosion casting to examine vessel remodeling. Risau and co-workers were the first to distinguish between two different mechanisms of embryonic blood vessel formation: vasculogenesis, the development of blood vessels from in situ differentiating endothelial cells and ungiogenesis, the sprouting of capillaries from preexisting vessels. Blockage and transplantation studies have been used to demonstrate the important role of Angioblast migration in both of these mechanisms. These studies are discussed in detail in this chapter. Noden has also found evidence from grafting experiments for a subset of invasive Angioblasts in the head that migrate extensively as individual cells initially unlabeled by QH-1 or related antibodies. The formation of dorsal aortae, intersomitic arteries, and endocardium has been followed in mouse embryos using a fluorescent lectin and antisera against von Willebrand factor. Serial sections, reconstructions, and scanning electron microscopy have been used to carefully examine the origin of the endocardium as a single tube in mouse embryos, particularly in relation to the foldings of the embryo that accompany heart formation.
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Endothelial cell origin and migration in embryonic heart and cranial blood vessel development
The Anatomical record, 1991Co-Authors: J. Douglas, Thomas J. PooleAbstract:Using the QH-1 monoclonal antibody as a marker for quail endothelium, blockage and transplant experiments were carried out to construct fate maps for the embryonic endocardium, to determine whether preendocardial Angioblasts are migratory, and, if these cells are migratory, to outline the pathways that they use for directed migration in embryonic blood vessel development. Recent descriptive studies using QH-1 to make immunofluorescent whole mounts have described a sequence of events leading to the establishment of the embryonic heart tube. These reports suggest that the pattern for the endocardium and cranial vasculature is established by migrating Angioblasts that form vascular cords which mature into blood vessels. Blockage experiments showed that the ventrolateral edge of the anterior intestinal portal serves as a substrate for the directed migration of pre-endocardial Angioblasts and that the pattern of the cranioventral vasculature forms independent of the source of Angioblasts. Transplant experiments showed that the origin for endocardial Angioblasts lies in mesodermal tissue just anterior to Henson's node, that these cells undergo directed migration to the pericardial area, and that Angioblasts are pluripotent with the ability to form different blood vessels. The transplant studies also showed that the embryonic mesoderm may contribute to extraembryonic blood vessels on the embryonic yolksac. These results support the hypothesis that embryonic blood vessels may develop by either the vasculogenesis or by the angiogenesis mechanism, and show that the endocardium of the primitive heart tube forms by vasculogenesis.