Cardiovascular System - Blood Vessel Development: Difference between revisions
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* '''Reconstructing the Vascular Developmental Milieu In Vitro'''{{#pmid:31718894|PMID31718894}} "Understanding human development has fascinated scientists for centuries. With advancements in stem cell technologies, this understanding has expanded beyond fascination to application towards informing the design of therapeutics in regenerative medicine. A focus on establishing a better grasp of the physicochemical cues governing differentiation and tissue assembly has continually enhanced engineered systems to an unprecedented level of biomimicry and, in doing so, has allowed the design of novel therapeutics. The vasculature has a critical role during early stages of development and regeneration events, and is responsive to a range of dynamic environmental cues. In this review, we present biomaterials systems capable of spatially and temporally controlling environmental signals that guide vascular fate and assembly, thereby further informing our understanding of differentiation schema." | |||
* '''Review - Molecular identity of arteries, veins, and lymphatics'''{{#pmid:30154011|PMID30154011}} "Arteries, veins, and lymphatic vessels are distinguished by structural differences that correspond to their different functions. Each of these vessels is also defined by specific molecular markers that persist throughout adult life; these markers are some of the molecular determinants that control the differentiation of embryonic undifferentiated cells into arteries, veins, or lymphatics. The Eph-B4 receptor and its ligand, ephrin-B2, are critical molecular determinants of vessel identity, arising on endothelial cells early in embryonic development. Eph-B4 and ephrin-B2 continue to be expressed on adult vessels and mark vessel identity. However, after vascular surgery, vessel identity can change and is marked by altered Eph-B4 and ephrin-B2 expression. Vein grafts show loss of venous identity, with less Eph-B4 expression. Arteriovenous fistulas show gain of dual arterial-venous identity, with both Eph-B4 and ephrin-B2 expression, and manipulation of Eph-B4 improves arteriovenous fistula patency. Patches used to close arteries and veins exhibit context-dependent gain of identity, that is, patches in the arterial environment gain arterial identity, whereas patches in the venous environment gain venous identity; these results show the importance of the host infiltrating cells in determining vascular identity after vascular surgery." | |||
* '''Erythro-myeloid progenitors can differentiate from endothelial cells and modulate embryonic vascular remodeling'''{{#pmid:28272478|PMID28272478}} "Erythro-myeloid progenitors (EMPs) were recently described to arise from the yolk sac endothelium, just prior to vascular remodeling, and are the source of adult/post-natal tissue resident macrophages. Questions remain, however, concerning whether EMPs differentiate directly from the endothelium or merely pass through. We provide the first evidence in vivo that EMPs can emerge directly from endothelial cells (ECs) and demonstrate a role for these cells in vascular development. We find that EMPs express most EC markers but late EMPs and EMP-derived cells do not take up acetylated low-density lipoprotein (AcLDL), as ECs do. When the endothelium is labelled with AcLDL before EMPs differentiate, EMPs and EMP-derived cells arise that are AcLDL+. If AcLDL is injected after the onset of EMP differentiation, however, the majority of EMP-derived cells are not double labelled. We find that cell division precedes entry of EMPs into circulation, and that blood flow facilitates the transition of EMPs from the endothelium into circulation in a nitric oxide-dependent manner. In gain-of-function studies, we inject the CSF1-Fc ligand in embryos and found that this increases the number of CSF1R+ cells, which localize to the venous plexus and significantly disrupt venous remodeling. This is the first study to definitively establish that EMPs arise from the endothelium in vivo and show a role for early myeloid cells in vascular development." | * '''Erythro-myeloid progenitors can differentiate from endothelial cells and modulate embryonic vascular remodeling'''{{#pmid:28272478|PMID28272478}} "Erythro-myeloid progenitors (EMPs) were recently described to arise from the yolk sac endothelium, just prior to vascular remodeling, and are the source of adult/post-natal tissue resident macrophages. Questions remain, however, concerning whether EMPs differentiate directly from the endothelium or merely pass through. We provide the first evidence in vivo that EMPs can emerge directly from endothelial cells (ECs) and demonstrate a role for these cells in vascular development. We find that EMPs express most EC markers but late EMPs and EMP-derived cells do not take up acetylated low-density lipoprotein (AcLDL), as ECs do. When the endothelium is labelled with AcLDL before EMPs differentiate, EMPs and EMP-derived cells arise that are AcLDL+. If AcLDL is injected after the onset of EMP differentiation, however, the majority of EMP-derived cells are not double labelled. We find that cell division precedes entry of EMPs into circulation, and that blood flow facilitates the transition of EMPs from the endothelium into circulation in a nitric oxide-dependent manner. In gain-of-function studies, we inject the CSF1-Fc ligand in embryos and found that this increases the number of CSF1R+ cells, which localize to the venous plexus and significantly disrupt venous remodeling. This is the first study to definitively establish that EMPs arise from the endothelium in vivo and show a role for early myeloid cells in vascular development." | ||
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* '''The relationship between human placental morphometry and ultrasonic measurements of utero-placental blood flow and fetal growth'''{{#pmid:26907381|PMID26907381}} "Placental area and weight are associated with uterine and umbilical blood flow, respectively, and both are associated with fetal growth rate." | * '''The relationship between human placental morphometry and ultrasonic measurements of utero-placental blood flow and fetal growth'''{{#pmid:26907381|PMID26907381}} "Placental area and weight are associated with uterine and umbilical blood flow, respectively, and both are associated with fetal growth rate." | ||
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| [[File:Mark_Hill.jpg|90px|left]] {{Most_Recent_Refs}} | | [[File:Mark_Hill.jpg|90px|left]] {{Most_Recent_Refs}} | ||
Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Blood+Vessel+Embryology ''Blood Vessel Embryology''] | Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Blood+Vessel+Development ''Blood Vessel Development''] [http://www.ncbi.nlm.nih.gov/pubmed/?term=Blood+Vessel+Embryology ''Blood Vessel Embryology''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Capillary+Development ''Capillary Development''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Artery+Development ''Artery Development''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Vein+Development ''Vein Development''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Endothelium+Development ''Endothelium Development''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Vascular+Smooth+Muscle+Development ''Vascular Smooth Muscle Development''] | ||
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* '''Cell-matrix signals specify bone endothelial cells during developmental osteogenesis'''{{#pmid:28218908|PMID28218908}} “Blood vessels in the mammalian skeletal system control bone formation and support haematopoiesis by generating local niche environments. Here, we report that embryonic and early postnatal long bone contains a specialized endothelial cell subtype, termed type E, which strongly supports osteoblast lineage cells and later gives rise to other endothelial cell subpopulations. The differentiation and functional properties of bone endothelial cells require cell-matrix signalling interactions." [[Musculoskeletal_System_-_Bone_Development|Bone Development]] | [https://omim.org/entry/135630 INTEGRIN BETA-1] | |||
* '''Endothelium in the {{pharyngeal arch}}es 3, 4 and 6 is derived from the second heart field'''{{#pmid:27955943|PMID27955943}} "Oxygenated blood from the heart is directed into the systemic circulation through the aortic arch arteries (AAAs). The AAAs arise by remodeling of three symmetrical pairs of {{pharyngeal arch}} arteries (PAAs), which connect the heart with the paired dorsal aortae at mid-gestation. Aberrant PAA formation results in defects frequently observed in patients with lethal congenital heart disease. How the PAAs form in mammals is not understood. The work presented in this manuscript shows that the second heart field (SHF) is the major source of progenitors giving rise to the endothelium of the pharyngeal arches 3 - 6, while the endothelium in the pharyngeal arches 1 and 2 is derived from a different source. During the formation of the PAAs 3 - 6, endothelial progenitors in the SHF extend cellular processes toward the pharyngeal endoderm, migrate from the SHF and assemble into a uniform vascular plexus. This plexus then undergoes remodeling, whereby plexus endothelial cells coalesce into a large PAA in each pharyngeal arch." | |||
* '''Review - The Molecular Regulation of Arteriovenous Specification and Maintenance'''{{#pmid:25641373|PMID25641373}} "The formation of a hierarchical vascular network, composed of arteries, veins and capillaries, is essential for embryogenesis and is required for the production of new functional vasculature in the adult. Elucidating the molecular mechanisms that orchestrate the differentiation of vascular endothelial cells into arterial and venous cell fates is requisite for regenerative medicine, as the directed formation of perfused vessels is desirable in a myriad of pathological settings, such as in diabetes and following myocardial infarction. Additionally, this knowledge will enhance our understanding and treatment of vascular anomalies, such as arteriovenous malformations (AVMs). From studies in vertebrate model organisms, such as mouse, zebrafish and chick, a number of key signaling pathways have been elucidated that are required for the establishment and maintenance of arterial and venous fates. These include the Hedgehog, Vascular Endothelial Growth Factor (VEGF), Transforming Growth Factor-β (TGF-β), Wnt and Notch signaling pathways. In addition, a variety of transcription factor families acting downstream of-or in concert with-these signaling networks play vital roles in arteriovenous (AV) specification. These include Notch and Notch-regulated transcription factors (e.g. HEY and HES), SOX factors, Forkhead factors, β-Catenin, ETS factors and COUP-TFII. It is becoming apparent that AV specification is a highly coordinated process that involves the intersection and carefully orchestrated activity of multiple signaling cascades and transcriptional networks." | * '''Review - The Molecular Regulation of Arteriovenous Specification and Maintenance'''{{#pmid:25641373|PMID25641373}} "The formation of a hierarchical vascular network, composed of arteries, veins and capillaries, is essential for embryogenesis and is required for the production of new functional vasculature in the adult. Elucidating the molecular mechanisms that orchestrate the differentiation of vascular endothelial cells into arterial and venous cell fates is requisite for regenerative medicine, as the directed formation of perfused vessels is desirable in a myriad of pathological settings, such as in diabetes and following myocardial infarction. Additionally, this knowledge will enhance our understanding and treatment of vascular anomalies, such as arteriovenous malformations (AVMs). From studies in vertebrate model organisms, such as mouse, zebrafish and chick, a number of key signaling pathways have been elucidated that are required for the establishment and maintenance of arterial and venous fates. These include the Hedgehog, Vascular Endothelial Growth Factor (VEGF), Transforming Growth Factor-β (TGF-β), Wnt and Notch signaling pathways. In addition, a variety of transcription factor families acting downstream of-or in concert with-these signaling networks play vital roles in arteriovenous (AV) specification. These include Notch and Notch-regulated transcription factors (e.g. HEY and HES), SOX factors, Forkhead factors, β-Catenin, ETS factors and COUP-TFII. It is becoming apparent that AV specification is a highly coordinated process that involves the intersection and carefully orchestrated activity of multiple signaling cascades and transcriptional networks." | ||
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===Reviews=== | ===Reviews=== | ||
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{{#pmid:25641373}} | {{#pmid:25641373}} | ||
Latest revision as of 09:39, 4 December 2019
Embryology - 26 Apr 2024 Expand to Translate |
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Introduction
Blood develops initially within the core of "blood islands" in the mesoderm. During development, there follows a series of "relocations" of the stem cells to different organs within the embryo. In the adult, these stem cells are located in the bone marrow. At the time when blood first forms, there are no bones!
Note that blood vessel development is tightly coupled to development of other systems for example: osteogenesis (bone formation) that is dependent upon early capillary formation; endocrine development that requires blood vessels for hormone distribution.
Vasculogenesis | Angiogenesis |
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formation of new blood vessels (endothelium from mesoderm) |
formation of blood vessels from pre-existing vessels (occurs in development and adult) |
Angioblasts initially form small cell clusters (blood islands) within the embryonic and extraembryonic mesoderm. These blood islands extend and fuse together making a primordial vascular network. Within these islands the peripheral cells form endothelial cells while the core cells form blood cells (haemocytoblasts).
Recent work has shown that the formation of the initial endothelial tube is by a process of coalescence of cellular vacuoles within the developing endothelial cells, which fuse together without cytoplasmic mixing to form the blood vessel lumen.
See also the related pages: artery, vein, placenta vascular bed, coronary circulation.
Some Recent Findings
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More recent papers |
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Blood Vessel Development Blood Vessel Embryology | Capillary Development | Artery Development | Vein Development | Endothelium Development | Vascular Smooth Muscle Development |
Older papers |
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These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.
See also the Discussion Page for other references listed by year and References on this current page.
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Endothelial Progenitors
Recent work has shown that the formation of the initial endothelial tube is by a process of coalescence of cellular vacuoles within the developing endothelial cells, which fuse together without cytoplasmic mixing to form the blood vessel lumen.[12]
Endothelial Tube Formation
Vessel Specification
The following data is from a recent review.[9]
Arterial Specification
Factor | Function |
Shh | Loss of Shh results in lack of arterial identity in zebrafish. Shh acts upstream of VEGF. |
VEGF | VEGF acts downstream of Shh signaling to activate Notch via the PLCγ/ERK pathway in zebrafish. Mutant mice expressing only VEGF188 lack arterial differentiation. |
Nrp1 | Null mice display impaired arterial differentiation. Nrp1 is involved in a positive feedback loop of VEGF signaling. |
Notch | Notch acts downstream of Shh and VEGF signaling in zebrafish. Notch1; Notch4 mutant mice have abnormal vascular development. |
Dll4 | Null mice lack arterial specification. |
Dll1 | Null mice fail to maintain arterial identity. |
Hey1/2 (Grl) | Null mice lack arterial specification. Lack of grl in zebrafish results in loss of arterial specification. |
Foxc1/c2 | Foxc1; Foxc2 mutant mice lack arterial specification. Foxc1 and Foxc2 directly regulate Dll4 and Hey2 expression. Foxc1 and Foxc2 are also involved in lymphatic vessel development. |
Sox7/18 | Lack of Sox7/18 results in loss of arterial identity in zebrafish. |
Snrk-1 | Snrk-1 acts downstream or parallel to Notch signaling in zebrafish. |
Dep1 | Dep1 acts upstream of PI3K in arterial specification in zebrafish. |
Crlr | Shh regulates VEGF activity by controlling crlr expression in zebrafish. |
EphrinB2 | Null mice lack boundaries between arteries and veins. EphrinB2 is involved in lymphatic vascular remodeling and maturation. |
Venous Specification
Factor | Function |
COUP-TFII | COUP-TFII suppresses arterial cell fate by inhibiting Nrp1 and Notch. COUP-TFII also interacts with Prox1 to regulate lymphatic gene expression. |
EphB4 | Null mice lack boundaries between arteries and veins. |
Lymphatic Specification
Factor | Function |
Sox18 | Null mice fail to specify lymphatic endothelial cells. Sox18 induces Prox1 expression. |
Prox1 | Prox1 induces lymphatic markers and maintains lymphatic cell identity. |
Vascular Endothelial Growth Factor
Growing blood vessels follow a gradient generated by tagret tissues/regions of Vascular Endothelial Growth Factor (VEGF) to establish a vascular bed. Recent findings suggest that Notch signaling acts as an inhibitor for this system, preventing sprouting of blood vessels.
Notch is a transmembrane receptor protein involved in regulating cell differentiation in many developing systems.
Notch and yolk sac blood vessels model[13] | Vasculogenesis and angiogenesis[14] |
Links: OMIM - VEGFA | OMIM - Notch
Regulators of Growth
The following data is from a review article on ovary vascular development.[15]
Stimulators of Angiogenisis
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Inhibitors of Angiogenisis
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Histology
Vein Light Microscopy
The entire developing and adult cardiovascular system (blood vessels and heart) is lined by a simple squamous epithelium. (Stain - Haematoxylin Eosin)
Capillaries
Type H
A developmental capillary endothelial cell subtype associated with osteogenesis, located at the metaphysis and endosteum of postnatal long bone, that couples angiogenesis with osteogenesis. This endothelial cell subtype expresses the markers CD31/PECAM1 and endomucin (CD31hi Emcnhi).
Type E
A newly identified endothelial cell subtype similar to type H in function, supporting osteoblast lineage cells and then gives rise to other endothelial cell subpopulations, but this subtype is found in embryonic and early postnatal long bone.[6]
Electron Micrographs
endothelium detail[16]
Arteries
Cardiac Blood Vessels
Earliest vessels in the heart wall develop subepicardially (beneath the outside surface of the heart) near the apex at Carnegie stage 15, which then extends centripetally and at stage 17 coronary arterial stems communicate with the aortic lumen.[17]
Abnormalities
Due to the extensive embryonic, and ongoing, remodelling of the vascular system, there are many different vascular variations and anomalies.
Neural
Persistent trigeminal and hypoglossal arteries[18]
- Links: Cerebrum Development | Head Development
References
- ↑ Blatchley MR & Gerecht S. (2019). Reconstructing the Vascular Developmental Milieu In Vitro. Trends Cell Biol. , , . PMID: 31718894 DOI.
- ↑ Wolf K, Hu H, Isaji T & Dardik A. (2019). Molecular identity of arteries, veins, and lymphatics. J. Vasc. Surg. , 69, 253-262. PMID: 30154011 DOI.
- ↑ Kasaai B, Caolo V, Peacock HM, Lehoux S, Gomez-Perdiguero E, Luttun A & Jones EA. (2017). Erythro-myeloid progenitors can differentiate from endothelial cells and modulate embryonic vascular remodeling. Sci Rep , 7, 43817. PMID: 28272478 DOI.
- ↑ Ashwell KW & Shulruf B. (2015). Quantitative comparison of cerebral artery development in human embryos with other eutherians. J. Anat. , 227, 286-96. PMID: 26183939 DOI.
- ↑ Salavati N, Sovio U, Mayo RP, Charnock-Jones DS & Smith GC. (2016). The relationship between human placental morphometry and ultrasonic measurements of utero-placental blood flow and fetal growth. Placenta , 38, 41-8. PMID: 26907381 DOI.
- ↑ 6.0 6.1 Langen UH, Pitulescu ME, Kim JM, Enriquez-Gasca R, Sivaraj KK, Kusumbe AP, Singh A, Di Russo J, Bixel MG, Zhou B, Sorokin L, Vaquerizas JM & Adams RH. (2017). Cell-matrix signals specify bone endothelial cells during developmental osteogenesis. Nat. Cell Biol. , 19, 189-201. PMID: 28218908 DOI.
- ↑ Wang X, Chen D, Chen K, Jubran A, Ramirez A & Astrof S. (2017). Endothelium in the pharyngeal arches 3, 4 and 6 is derived from the second heart field. Dev. Biol. , 421, 108-117. PMID: 27955943 DOI.
- ↑ Fish JE & Wythe JD. (2015). The molecular regulation of arteriovenous specification and maintenance. Dev. Dyn. , 244, 391-409. PMID: 25641373 DOI.
- ↑ 9.0 9.1 Kume T. (2010). Specification of arterial, venous, and lymphatic endothelial cells during embryonic development. Histol. Histopathol. , 25, 637-46. PMID: 20238301 DOI.
- ↑ Wasteson P, Johansson BR, Jukkola T, Breuer S, Akyürek LM, Partanen J & Lindahl P. (2008). Developmental origin of smooth muscle cells in the descending aorta in mice. Development , 135, 1823-32. PMID: 18417617 DOI.
- ↑ High FA, Lu MM, Pear WS, Loomes KM, Kaestner KH & Epstein JA. (2008). Endothelial expression of the Notch ligand Jagged1 is required for vascular smooth muscle development. Proc. Natl. Acad. Sci. U.S.A. , 105, 1955-9. PMID: 18245384 DOI.
- ↑ Reyes M, Dudek A, Jahagirdar B, Koodie L, Marker PH & Verfaillie CM. (2002). Origin of endothelial progenitors in human postnatal bone marrow. J. Clin. Invest. , 109, 337-46. PMID: 11827993 DOI.
- ↑ Copeland JN, Feng Y, Neradugomma NK, Fields PE & Vivian JL. (2011). Notch signaling regulates remodeling and vessel diameter in the extraembryonic yolk sac. BMC Dev. Biol. , 11, 12. PMID: 21352545 DOI.
- ↑ Takuwa Y, Du W, Qi X, Okamoto Y, Takuwa N & Yoshioka K. (2010). Roles of sphingosine-1-phosphate signaling in angiogenesis. World J Biol Chem , 1, 298-306. PMID: 21537463 DOI.
- ↑ Augustin HG. (2000). Vascular morphogenesis in the ovary. Baillieres Best Pract Res Clin Obstet Gynaecol , 14, 867-82. PMID: 11141338 DOI.
- ↑ Detry B, Bruyère F, Erpicum C, Paupert J, Lamaye F, Maillard C, Lenoir B, Foidart JM, Thiry M & Noël A. (2011). Digging deeper into lymphatic vessel formation in vitro and in vivo. BMC Cell Biol. , 12, 29. PMID: 21702933 DOI.
- ↑ Turner K & Navaratnam V. (1996). The positions of coronary arterial ostia. Clin Anat , 9, 376-80. PMID: 8915616 <376::AID-CA3>3.0.CO;2-9 DOI.
- ↑ Menshawi K, Mohr JP & Gutierrez J. (2015). A Functional Perspective on the Embryology and Anatomy of the Cerebral Blood Supply. J Stroke , 17, 144-58. PMID: 26060802 DOI.
Reviews
Wolf K, Hu H, Isaji T & Dardik A. (2019). Molecular identity of arteries, veins, and lymphatics. J. Vasc. Surg. , 69, 253-262. PMID: 30154011 DOI.
Fish JE & Wythe JD. (2015). The molecular regulation of arteriovenous specification and maintenance. Dev. Dyn. , 244, 391-409. PMID: 25641373 DOI.
Articles
Davidson AJ & Zon LI. (2000). Turning mesoderm into blood: the formation of hematopoietic stem cells during embryogenesis. Curr. Top. Dev. Biol. , 50, 45-60. PMID: 10948449
McGrath KE, Koniski AD, Malik J & Palis J. (2003). Circulation is established in a stepwise pattern in the mammalian embryo. Blood , 101, 1669-76. PMID: 12406884 DOI.
Search Pubmed
Click on the listed keywords below (used to search the external database) the most current references on Medline will be displayed.
Search Pubmed: Blood Vessel Development | Blood Vessel embryology | Blood Vessel smooth muscle Development | Blood Vessel smooth muscle Development
Terms
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Cardiovascular System Development See also Heart terms, Immune terms and Blood terms.
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Cite this page: Hill, M.A. (2024, April 26) Embryology Cardiovascular System - Blood Vessel Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Blood_Vessel_Development
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G