Vascularization in the murine allantois occurs by vasculogenesis without accompanying erythropoiesis

Development ◽  
1998 ◽  
Vol 125 (22) ◽  
pp. 4507-4520 ◽  
Author(s):  
K.M. Downs ◽  
S. Gifford ◽  
M. Blahnik ◽  
R.L. Gardner

The aim of this study was to determine whether the blood vessels of the murine allantois are formed by vasculogenesis or angiogenesis. Morphological analysis revealed that differentiation of allantoic mesoderm into an outer layer of mesothelium and an inner vascular network begins in the distal region of the allantois, which is most remote from other tissues, as early as the late neural plate stage (approximately 7.75 days postcoitum). Nascent blood vessels were not found in the base of the allantois until 4-somite pairs had formed in the fetus (approximately 8.25 days postcoitum), and vascular continuity with the yolk sac and fetus was not present until the 6-somite-pair stage (approximately 8.5 days postcoitum). Immunohistochemical analysis demonstrated that flk-1, a molecular marker of early endothelial cells, is expressed in significantly more distal than basal core cells in the early allantois and never in mesothelium. Furthermore, synchronous grafting of donor yolk sac containing blood islands into blood islands of headfold-stage host conceptuses provided no evidence that the yolk sac contributes endothelial cells to the allantois. Finally, when removed from conceptuses and cultured in isolation, neural plate and headfold-stage allantoises formed a conspicuous vascular network that was positive for Flk-1. Hence, the vasculature of the allantois is formed intrinsically by vasculogenesis rather than extrinsically via angiogenesis from the adjacent yolk sac or fetus. Whether allantoic vasculogenesis is associated with erythropoiesis was also investigated. Benzidine-staining in situ revealed that primitive erythroid cells were not identified in the allantois until 6-somite pairs when continuity between its vasculature and that of the yolk sac was first evident. Nevertheless, a small number of allantoises removed from conceptuses at a considerably earlier stage were found to contain erythroid precursor cells following culture in isolation. To determine whether such erythroid cells could be of allantoic origin, host allantoises were made chimeric with lacZ-expressing donor allantoises that were additionally labeled with [3H]methyl thymidine. Following culture and autoradiography, many lacZ-expressing benzidine-stained cells were observed in donor allantoises, but none contained silver grains above background. Moreover, no cells of donor allantoic origin were found in the fetus or yolk sac. Hence, vasculogenesis seems to be independent of erythropoiesis in the allantois and to involve a distal-to-proximal gradient in differentiation of allantoic mesoderm into the endothelial cell lineage. Furthermore, this gradient is established earlier than reported previously, being present at the neural plate stage.

Blood ◽  
1995 ◽  
Vol 86 (1) ◽  
pp. 156-163 ◽  
Author(s):  
J Palis ◽  
KE McGrath ◽  
PD Kingsley

The blood islands of the visceral yolk sac (VYS) are the initial sites of hematopoiesis in mammals. We have developed a yolk sac explant culture system to study the process of blood cell and endothelial cell development from extraembryonic mesoderm cells. No benzidine-positive cells or beta H1-globin mRNA expression was detected at the primitive streak or neural plate stage of development (E7.5). However, when isolated E7.5 dissected tissues were cultured for 36 to 72 hours in serum-free medium, hundreds of hemoglobin-producing cells and embryonic globin gene expression were identified in both intact yolk sac and VYS mesoderm explants. Explanted E7.5 extraembryonic mesoderm tissues thus recapitulate in vivo primitive erythropoiesis and do not require the presence of a vascular network or the VYS endoderm. Yolk sac blood islands also contain endothelial cells that arise by vasculogenesis and express flk-1. We detected flk-1 mRNA as early as the primitive streak stage of mouse embryogenesis. Culture of embryo proper and intact VYS explants, which contain both mesoderm and endoderm cells, produced capillary networks and expressed flk-1. In contrast, vascular networks were not seen when VYS mesoderm was cultured alone, although flk-1 expression was similar to that of intact VYS explants. The addition of vascular endothelial growth factor to VYS mesoderm explants did not induce vascular network formation. These results suggest that the VYS endoderm or its extracellular matrix is necessary for the coalescence of developing endothelial cells into capillary networks.


2020 ◽  
Vol 65 (No. 1) ◽  
pp. 36-40
Author(s):  
R Morais ◽  
AP Maurique ◽  
J Villela ◽  
L Sonne ◽  
B Anjos

A male Polwarth lamb with a good body score was born with a pendulous, oval, red mass adhering to the skin in the left ventrolateral thoracic area. The nodule was removed when the lamb was five days old and sent for a gross and histopathological evaluation. Macroscopically, the mass was reddish, slightly oval and flat, well delineated, and contained a central ulcerated area. Microscopically, it showed a marked proliferation of well-differentiated endothelial cells with the formation of new blood vessels. An immunohistochemical analysis showed mild cytoplasmic immunostaining for the von Willebrand Factor in the endothelial cells. To the best of our knowledge, this is the first report of a cutaneous vascular hamartoma in a sheep.


Development ◽  
2002 ◽  
Vol 129 (2) ◽  
pp. 361-372 ◽  
Author(s):  
Noah Byrd ◽  
Sandy Becker ◽  
Peter Maye ◽  
Roopa Narasimhaiah ◽  
Benoit St-Jacques ◽  
...  

Blood islands, the precursors of yolk sac blood vessels, contain primitive erythrocytes surrounded by a layer of endothelial cells. These structures differentiate from extra-embryonic mesodermal cells that underlie the visceral endoderm. Our previous studies have shown that Indian hedgehog (Ihh) is expressed in the visceral endoderm both in the visceral yolk sac in vivo and in embryonic stem (ES) cell-derived embryoid bodies. Differentiating embryoid bodies form blood islands, providing an in vitro model for studying vasculogenesis and hematopoiesis. A role for Ihh in yolk sac function is suggested by the observation that roughly 50% of Ihh–/– mice die at mid-gestation, potentially owing to vascular defects in the yolk sac. To address the nature of the possible vascular defects, we have examined the ability of ES cells deficient for Ihh or smoothened (Smo), which encodes a receptor component essential for all hedgehog signaling, to form blood islands in vitro. Embryoid bodies derived from these cell lines are unable to form blood islands, and express reduced levels of both PECAM1, an endothelial cell marker, and α-SMA, a vascular smooth muscle marker. RT-PCR analysis in the Ihh–/– lines shows a substantial decrease in the expression of Flk1 and Tal1, markers for the hemangioblast, the precursor of both blood and endothelial cells, as well as Flt1, an angiogenesis marker. To extend these observations, we have examined the phenotypes of embryo yolk sacs deficient for Ihh or Smo. Whereas Ihh–/– yolk sacs can form blood vessels, the vessels are fewer in number and smaller, perhaps owing to their inability to undergo vascular remodeling. Smo–/– yolk sacs arrest at an earlier stage: the endothelial tubes are packed with hematopoietic cells, and fail to undergo even the limited vascular remodeling observed in the Ihh–/– yolk sacs. Our study supports a role for hedgehog signaling in yolk sac angiogenesis.


Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 471-478 ◽  
Author(s):  
W. Risau ◽  
H. Sariola ◽  
H.G. Zerwes ◽  
J. Sasse ◽  
P. Ekblom ◽  
...  

Embryonic stem cells (ESC) have been established previously from the inner cell mass cells of mouse blastocysts. In suspension culture, they spontaneously differentiate to blood-island-containing cystic embryoid bodies (CEB). The development of blood vessels from in situ differentiating endothelial cells of blood islands, a process which we call vasculogenesis, was induced by injecting ESC into the peritoneal cavity of syngeneic mice. In the peritoneum, fusion of blood islands and formation of an in vivo-like primary capillary plexus occurred. Transplantation of ESC and ESC-derived complex and cystic embryoid bodies (ESC-CEB) onto the quail chorioallantoic membrane (CAM) induced an angiogenic response, which was directed by nonyolk sac endoderm structures. Neither yolk sac endoderm from ESC-CEB nor normal mouse yolk sac tissue induced angiogenesis on the quail CAM. Extracts from ESC-CEB stimulated the proliferation of capillary endothelial cells in vitro. Mitogenic activity increase during in vitro culture and differentiation of ESC. Almost all growth factor activity was associated with the cells. The ESC-CEB derived endothelial cell growth factor bound to heparin-sepharose. The identification of acidic fibroblast growth factor (FGF)in heparin-sepharose-purified material was accomplished by immunoblot experiments involving antibodies against acidic and basic FGF. We conclude that vasculogenesis, the development of blood vessels from in situ differentiating endothelial cells, and angiogenesis, the sprouting of capillaries from preexisting vessels are very early events during embryogenesis which can be studied using ESC differentiating in vitro. Our results suggest that vasculogenesis and angiogenesis are differently regulated.


Author(s):  
Chaojie Wang ◽  
Yandong Gong ◽  
Anbang Wei ◽  
Tao Huang ◽  
Siyuan Hou ◽  
...  

Nature ◽  
1978 ◽  
Vol 271 (5642) ◽  
pp. 246-248 ◽  
Author(s):  
H. R. CARNE ◽  
ELEANOR O. ONON

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria I. Alvarez-Vergara ◽  
Alicia E. Rosales-Nieves ◽  
Rosana March-Diaz ◽  
Guiomar Rodriguez-Perinan ◽  
Nieves Lara-Ureña ◽  
...  

AbstractThe human Alzheimer’s disease (AD) brain accumulates angiogenic markers but paradoxically, the cerebral microvasculature is reduced around Aß plaques. Here we demonstrate that angiogenesis is started near Aß plaques in both AD mouse models and human AD samples. However, endothelial cells express the molecular signature of non-productive angiogenesis (NPA) and accumulate, around Aß plaques, a tip cell marker and IB4 reactive vascular anomalies with reduced NOTCH activity. Notably, NPA induction by endothelial loss of presenilin, whose mutations cause familial AD and which activity has been shown to decrease with age, produced a similar vascular phenotype in the absence of Aß pathology. We also show that Aß plaque-associated NPA locally disassembles blood vessels, leaving behind vascular scars, and that microglial phagocytosis contributes to the local loss of endothelial cells. These results define the role of NPA and microglia in local blood vessel disassembly and highlight the vascular component of presenilin loss of function in AD.


Author(s):  
Francesca Pagani ◽  
Elisa Tratta ◽  
Patrizia Dell’Era ◽  
Manuela Cominelli ◽  
Pietro Luigi Poliani

AbstractEarly B-cell factor-1 (EBF1) is a transcription factor with an important role in cell lineage specification and commitment during the early stage of cell maturation. Originally described during B-cell maturation, EBF1 was subsequently identified as a crucial molecule for proper cell fate commitment of mesenchymal stem cells into adipocytes, osteoblasts and muscle cells. In vessels, EBF1 expression and function have never been documented. Our data indicate that EBF1 is highly expressed in peri-endothelial cells in both tumor vessels and in physiological conditions. Immunohistochemistry, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and fluorescence-activated cell sorting (FACS) analysis suggest that EBF1-expressing peri-endothelial cells represent bona fide pericytes and selectively express well-recognized markers employed in the identification of the pericyte phenotype (SMA, PDGFRβ, CD146, NG2). This observation was also confirmed in vitro in human placenta-derived pericytes and in human brain vascular pericytes (HBVP). Of note, in accord with the key role of EBF1 in the cell lineage commitment of mesenchymal stem cells, EBF1-silenced HBVP cells showed a significant reduction in PDGFRβ and CD146, but not CD90, a marker mostly associated with a prominent mesenchymal phenotype. Moreover, the expression levels of VEGF, angiopoietin-1, NG2 and TGF-β, cytokines produced by pericytes during angiogenesis and linked to their differentiation and activation, were also significantly reduced. Overall, the data suggest a functional role of EBF1 in the cell fate commitment toward the pericyte phenotype.


Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 751-758 ◽  
Author(s):  
M Bondurant ◽  
M Koury ◽  
SB Krantz ◽  
T Blevins ◽  
DT Duncan

Abstract Murine erythroid precursor cells, stimulated to proliferate in vitro in the absence of added erythropoietin (EP) by the anemia strain of Friend virus (FVA), will subsequently respond to EP by complete erythrocyte differentiation. If not exposed to EP, the erythroid cells divide for about 120 hr in culture, and they maintain the potential for full differentiation in response to EP added at any time during the period from 72 to 120 hr. Between 96 and 120 hr of culture without added EP, the EP-sensitive erythroid precursor cells that have formed discrete erythroid bursts can be isolated in relatively large numbers from such cultures by plucking with a Pasteur pipette. The addition of EP initiates the final stages of erythroid differentiation, including heme synthesis in 70%-80% of these isolated cells. With respect to homogeneity of the precursor cells, quantity of EP-responsive cells obtainable, and uniformity of EP responsiveness, this system is uniquely favorable for biochemical studies of the late differentiation effects of EP. The overall changes in gene expression accompanying EP- induced terminal differentiation were examined by two-dimensional gel electrophoresis of proteins labeled for a short time with radioactive amino acids. Several new proteins are synthesized in these erythroid cells during terminal differentiation, but the number is a very small percentage of the total number of proteins being made. Thus, in this system, the effect of EP is to initiate expression of a small group of genes, including those for globins, spectrin, and other proteins involved in the final stages of erythroid differentiation.


1960 ◽  
Vol 11 (3) ◽  
pp. 365 ◽  
Author(s):  
CW Stump ◽  
JP Robins ◽  
ML Garde

The material consists of 20 embryos (5-30 mm) and two foetuses (63 mm and 90 mm) collected at whaling stations on Moreton and Norfolk Islands (latitude 27� 11'S. and 29� 5' S. respectively) during late August, September, and early October in 1952-53-54 and 1956. The consecutive series permitted the study of membrane formation and organogenesis. Younger embryos are found in grooves between the folds of endometrium in a constant site in that uterine horn associated with the ovary containing the recent corpus luteum. Older embryos and the early foetus are adapted to lie freely in the uterine fluid, and are devoid of any mechanism for apposition or attachment to the endometrium. Variation in the sequence of the association of the components of the umbilical cord provides suspensory structures for the amnion and yolk sac, and for the embryo a bifid ligament, retained in the early foetus for attachment of the foetal membranes. In the younger foetus the allantoic duct drains the nephric secretion into the uterine cavity. In the older foetus chorionic villi are present. The bifid suspensory ligament forms the major part of the distal region of the umbilical cord. The allantoic duct is reunited with the allantoic sac. Amniogenesis is by folding. During the embryonic period the chorio-amniotic connection forms a suspensory ligament. The yolk sac, attached by a novel ligament to the amnion, is large and functional in the embryo. In the foetus vascular splanchnopleure is present in a tubular form. A rete system develops in the embryo.


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