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  1. Article: Formation of the coronary vasculature during development.

    Tomanek, Robert J

    Angiogenesis

    2005  Volume 8, Issue 3, Page(s) 273–284

    Abstract: The formation of the coronary vasculature involves a series of carefully regulated temporal events ... remodeling. Coronary endothelial, smooth muscle and fibroblast cells differentiate via ... to form the two ostia. Smooth muscle cell recruitment occurs rapidly and the coronary artery network ...

    Abstract The formation of the coronary vasculature involves a series of carefully regulated temporal events that include vasculogenesis, angiogenesis, arteriogenesis and remodeling. This review explores these events, which begin with the migration of proepicardial cells to form the epicardium and end with postnatal growth and remodeling. Coronary endothelial, smooth muscle and fibroblast cells differentiate via epithelial-mesenchymal transformation; these cells delaminate from the epicardium. Following the formation of a tubular network by endothelial cells, an aortic ring of endothelial cells penetrates the aorta at the left and right aortic cusps to form the two ostia. Smooth muscle cell recruitment occurs rapidly and the coronary artery network begins forming as blood flow is established. Recent studies have identified a number of regulatory molecules that play key roles in epicardial formation and the transformation of its component cells into mesenchyme. Moreover, we are finally gaining some understanding regarding the interplay of angiogenic growth factors in the complex process of establishing the coronary vascular tree. Understanding coronary embryogenesis is important for interventions regarding adult cardiovascular diseases as well as those necessary to correct congenital defects.
    MeSH term(s) Cell Differentiation/physiology ; Coronary Vessels/embryology ; Coronary Vessels/growth & development ; Endothelial Cells/physiology ; Endothelial Growth Factors/metabolism ; Humans ; Models, Biological ; Muscle, Smooth/physiology ; Neovascularization, Physiologic/physiology
    Chemical Substances Endothelial Growth Factors
    Language English
    Publishing date 2005
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 1484717-6
    ISSN 0969-6970
    ISSN 0969-6970
    DOI 10.1007/s10456-005-9014-9
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  2. Article ; Online: Coronary vessel formation in development and regeneration: origins and mechanisms.

    Tian, Xueying / Zhou, Bin

    Journal of molecular and cellular cardiology

    2022  Volume 167, Page(s) 67–82

    Abstract: ... sources and molecular mechanisms of coronary vessel formation during heart development and regeneration ... of how coronary vasculature is constructed and what developmental pathways might be reactivated after ... tracing studies of coronary vasculature have revealed multiple developmental origins for coronary ...

    Abstract Neovascularization of the ischemic myocardium following infarction is vital for the survival of cardiomyocytes and prevention of heart failure. However, the intrinsic revascularization following ischemic injury in the heart is inadequate to restore blood flow to the infarcted myocardium. A comprehensive understanding of how coronary vasculature is constructed and what developmental pathways might be reactivated after infarction is beneficial to develop effective strategies for heart revascularization. The latest lineage tracing studies of coronary vasculature have revealed multiple developmental origins for coronary vascular endothelial cells. The development and growth of coronary vessels emanated from different cellular origins are governed by distinct regulatory mechanisms. Here, we highlight recent research advancements on cellular sources and molecular mechanisms of coronary vessel formation during heart development and regeneration, and also elaborate on how these mechanisms can be reactivated or recapitulated to facilitate therapeutic revascularization in ischemic heart disease.
    MeSH term(s) Coronary Vessels ; Endothelial Cells ; Humans ; Infarction ; Myocardium ; Myocytes, Cardiac ; Neovascularization, Physiologic/physiology
    Language English
    Publishing date 2022-03-27
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2022.03.009
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  3. Article ; Online: Maternal and zygotic ZFP57 regulate coronary vascular formation and myocardium maturation in mouse embryo.

    Zhao, Junzheng / Zhao, Jingjie

    Developmental dynamics : an official publication of the American Association of Anatomists

    2022  Volume 253, Issue 1, Page(s) 144–156

    Abstract: ... to underdeveloped coronary vasculature, meanwhile, there was an ectopic overproduction of blood islands over ... that maternal and zygotic Zfp57 modulate NOTCH signaling during cardiac development. In this study ... we investigated Zfp57 mutants from E11.5 to E13.5 to delineate its function during cardiac development.: Results ...

    Abstract Background: Genomic and epigenomic dynamics both play critical roles during embryogenesis. Zfp57 maintains genomic imprinting with both maternal and zygotic functions. In our previous study, we found that maternal and zygotic Zfp57 modulate NOTCH signaling during cardiac development. In this study, we investigated Zfp57 mutants from E11.5 to E13.5 to delineate its function during cardiac development.
    Results: Here, we describe novel roles of maternal and zygotic Zfp57 during cardiovascular system development. We found that maternal and zygotic Zfp57 was required for coronary vascular development. Maternal and zygotic loss of Zfp57 perturbed the sprouting of the sinus venosus-derived endothelial cells and led to underdeveloped coronary vasculature, meanwhile, there was an ectopic overproduction of blood islands over the ventricles. Furthermore, loss of Zfp57 and failed vasculature disturbed myocardium maturation. Loss of maternal and zygotic Zfp57 resulted in hyper trabeculation and failed myocardium compaction. Zfp57 zygotic mutant (M
    Conclusions: Our results suggest that maternal and zygotic ZFP57 are essential for coronary vascular formation and myocardium maturation in mice. Our research provides evidence for the role of genomic imprinting during embryogenesis.
    MeSH term(s) Animals ; Mice ; DNA Methylation ; Endothelial Cells/metabolism ; Heart ; Myocardium/metabolism ; Repressor Proteins/genetics
    Chemical Substances Repressor Proteins ; Zfp-57 protein, mouse
    Language English
    Publishing date 2022-09-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.530
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  4. Article ; Online: Coronary vessel formation in development and disease: mechanisms and insights for therapy.

    Lupu, Irina-Elena / De Val, Sarah / Smart, Nicola

    Nature reviews. Cardiology

    2020  Volume 17, Issue 12, Page(s) 790–806

    Abstract: ... from developmental studies. Coronary vessels originate from multiple cellular sources during development and form ... to form a functional coronary vasculature. In this Review, we describe the latest advances ... in our understanding of the processes involved in coronary vessel formation, with mechanistic insights taken ...

    Abstract The formation of new blood vessels after myocardial infarction (MI) is essential for the survival of existing and regenerated cardiac tissue. However, the extent of endogenous revascularization after MI is insufficient, and MI can often result in ventricular remodelling, progression to heart failure and premature death. The neutral results of numerous clinical trials that have evaluated the efficacy of angiogenic therapy to revascularize the infarcted heart reflect our poor understanding of the processes required to form a functional coronary vasculature. In this Review, we describe the latest advances in our understanding of the processes involved in coronary vessel formation, with mechanistic insights taken from developmental studies. Coronary vessels originate from multiple cellular sources during development and form through a number of distinct and carefully orchestrated processes. The ectopic reactivation of developmental programmes has been proposed as a new paradigm for regenerative medicine, therefore, a complete understanding of these processes is crucial. Furthermore, knowledge of how these processes differ between the embryonic and adult heart, and how they might be more closely recapitulated after injury are critical for our understanding of regenerative biology, and might facilitate the identification of tractable molecular targets to therapeutically promote neovascularization and regeneration of the infarcted heart.
    MeSH term(s) Coronary Vessels/physiology ; Humans ; Myocardial Infarction/therapy ; Regeneration
    Language English
    Publishing date 2020-06-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-020-0400-1
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  5. Article ; Online: Mechanisms of Trabecular Formation and Specification During Cardiogenesis.

    Wu, Mingfu

    Pediatric cardiology

    2018  Volume 39, Issue 6, Page(s) 1082–1089

    Abstract: ... distinct from the cardiomyocytes in compact zone. Once the coronary vasculature system starts to function ... Trabecular morphogenesis is a key morphologic event during cardiogenesis and contributes ... to the formation of a competent ventricular wall. Lack of trabeculation results in embryonic lethality ...

    Abstract Trabecular morphogenesis is a key morphologic event during cardiogenesis and contributes to the formation of a competent ventricular wall. Lack of trabeculation results in embryonic lethality. The trabecular morphogenesis is a multistep process that includes, but is not limited to, trabecular initiation, proliferation/growth, specification, and compaction. Although a number of signaling molecules have been implicated in regulating trabeculation, the cellular processes underlying mammalian trabecular formation are not fully understood. Recent works show that the myocardium displays polarity, and oriented cell division (OCD) and directional migration of the cardiomyocytes in the monolayer myocardium are required for trabecular initiation and formation. Furthermore, perpendicular OCD is an extrinsic asymmetric cell division that contributes to trabecular specification, and is a mechanism that causes the trabecular cardiomyocytes to be distinct from the cardiomyocytes in compact zone. Once the coronary vasculature system starts to function in the embryonic heart, the trabeculae will coalesce with the compact zone to thicken the heart wall, and abnormal compaction will lead to left ventricular non-compaction (LVNC) and heart failure. There are many reviews about compaction and LVNC. In this review, we will focus on the roles of myocardial polarity and OCD in trabecular initiation, formation, and specification.
    MeSH term(s) Animals ; Heart Ventricles/cytology ; Heart Ventricles/embryology ; Heart Ventricles/growth & development ; Humans ; Mice ; Morphogenesis ; Myocytes, Cardiac/physiology
    Language English
    Publishing date 2018-03-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 800857-7
    ISSN 1432-1971 ; 0172-0643
    ISSN (online) 1432-1971
    ISSN 0172-0643
    DOI 10.1007/s00246-018-1868-x
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  6. Article ; Online: Vessel formation. De novo formation of a distinct coronary vascular population in neonatal heart.

    Tian, Xueying / Hu, Tianyuan / Zhang, Hui / He, Lingjuan / Huang, Xiuzhen / Liu, Qiaozhen / Yu, Wei / He, Liang / Yang, Zhen / Yan, Yan / Yang, Xiao / Zhong, Tao P / Pu, William T / Zhou, Bin

    Science (New York, N.Y.)

    2014  Volume 345, Issue 6192, Page(s) 90–94

    Abstract: ... vasculature. Our data show that lineage conversion of neonatal endocardial cells during trabecular compaction ... means of rapidly augmenting the coronary vasculature. This mechanism of postnatal coronary vascular ... The postnatal coronary vessels have been viewed as developing through expansion of vessels formed ...

    Abstract The postnatal coronary vessels have been viewed as developing through expansion of vessels formed during the fetal period. Using genetic lineage tracing, we found that a substantial portion of postnatal coronary vessels arise de novo in the neonatal mouse heart, rather than expanding from preexisting embryonic vasculature. Our data show that lineage conversion of neonatal endocardial cells during trabecular compaction generates a distinct compartment of the coronary circulation located within the inner half of the ventricular wall. This lineage conversion occurs within a brief period after birth and provides an efficient means of rapidly augmenting the coronary vasculature. This mechanism of postnatal coronary vascular growth provides avenues for understanding and stimulating cardiovascular regeneration following injury and disease.
    MeSH term(s) Animals ; Cell Lineage/genetics ; Coronary Vessels/growth & development ; Coronary Vessels/physiology ; Endocardium/cytology ; Endocardium/physiology ; Heart/growth & development ; Heart/physiology ; Mice ; Myocardium/cytology ; Neovascularization, Physiologic/genetics ; Neovascularization, Physiologic/physiology ; Regeneration
    Language English
    Publishing date 2014-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1251487
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  7. Article ; Online: CCBE1 is required for coronary vessel development and proper coronary artery stem formation in the mouse heart.

    Bonet, Fernando / Pereira, Paulo N G / Bover, Oriol / Marques, Sara / Inácio, José M / Belo, José A

    Developmental dynamics : an official publication of the American Association of Anatomists

    2018  Volume 247, Issue 10, Page(s) 1135–1145

    Abstract: ... However, whether CCBE1 plays a similar role during coronary vasculature development is still unknown. Here ... Background: Proper coronary vasculature development is essential for late-embryonic and adult ... we investigate the coronary vasculature development in Ccbe1 mutant embryos.: Results: We show that Ccbe1 is ...

    Abstract Background: Proper coronary vasculature development is essential for late-embryonic and adult heart function. The developmental regulation of coronary embryogenesis is complex and includes the coordinated activity of multiple signaling pathways. CCBE1 plays an important role during lymphangiogenesis, enhancing VEGF-C signaling, which is also required for coronary vasculature formation. However, whether CCBE1 plays a similar role during coronary vasculature development is still unknown. Here, we investigate the coronary vasculature development in Ccbe1 mutant embryos.
    Results: We show that Ccbe1 is expressed in the epicardium, like Vegf-c, and also in the sinus venosus (SV) at the stages of its contribution to coronary vasculature formation. We also report that absence of CCBE1 in cardiac tissue inhibited coronary growth that sprouts from the SV endocardium at the dorsal cardiac wall. This disruption of coronary formation correlates with abnormal processing of VEGF-C propeptides, suggesting VEGF-C-dependent signaling alteration. Moreover, Ccbe1 loss-of-function leads to the development of defective dorsal and ventral intramyocardial vessels. We also demonstrate that Ccbe1 mutants display delayed and mispatterned coronary artery (CA) stem formation.
    Conclusions: CCBE1 is essential for coronary vessel formation, independent of their embryonic origin, and is also necessary for peritruncal vessel growth and proper CA stem patterning. Developmental Dynamics 247:1135-1145, 2018. © 2018 Wiley Periodicals, Inc.
    MeSH term(s) Animals ; Calcium-Binding Proteins/metabolism ; Calcium-Binding Proteins/physiology ; Coronary Vessels/embryology ; Coronary Vessels/growth & development ; Heart/embryology ; Heart/growth & development ; Lymphangiogenesis ; Mice ; Pericardium/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/physiology ; Vascular Endothelial Growth Factor C/metabolism
    Chemical Substances Calcium-Binding Proteins ; Ccbe1 protein, mouse ; Tumor Suppressor Proteins ; Vascular Endothelial Growth Factor C
    Language English
    Publishing date 2018-09-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.24670
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  8. Article ; Online: The Epicardium and Coronary Artery Formation

    José M. Pérez-Pomares / Adriana A. S. Pires-Gomes

    Journal of Developmental Biology, Vol 1, Iss 3, Pp 186-

    2013  Volume 202

    Abstract: ... during coronary blood vessel embryonic development, contributing cells to the coronary vasculature ... The coronary system is the network of blood vessels that nourishes the heart muscle. After birth ... proper coronary blood circulation is required to support heart homeostasis, and altered coronary function ...

    Abstract The coronary system is the network of blood vessels that nourishes the heart muscle. After birth, proper coronary blood circulation is required to support heart homeostasis, and altered coronary function frequently leads to myocardial ischemia, infarction and heart failure. The epicardium plays a pivotal role during coronary blood vessel embryonic development, contributing cells to the coronary vasculature, but also secreting diffusible signals that regulate coronary morphogenesis and secondarily impact on ventricular compact myocardium growth. Accordingly, anomalous epicardium development gives rise to the multiple congenital defects of the coronary vascular system and the heart walls. In this review, we will summarize and discuss our current knowledge on the embryogenesis of coronary blood vessels, as related to epicardial development, and attempt to highlight the biomedical relevance of this tissue.
    Keywords coronary artery ; embryo ; heart vascularization ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2013-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
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  9. Article ; Online: Non-muscle myosin IIB (Myh10) is required for epicardial function and coronary vessel formation during mammalian development.

    Ridge, Liam A / Mitchell, Karen / Al-Anbaki, Ali / Shaikh Qureshi, Wasay Mohiuddin / Stephen, Louise A / Tenin, Gennadiy / Lu, Yinhui / Lupu, Irina-Elena / Clowes, Christopher / Robertson, Abigail / Barnes, Emma / Wright, Jayne A / Keavney, Bernard / Ehler, Elisabeth / Lovell, Simon C / Kadler, Karl E / Hentges, Kathryn E

    PLoS genetics

    2017  Volume 13, Issue 10, Page(s) e1007068

    Abstract: ... hearts also identified defects in the formation of the coronary vasculature. We attribute ... The coronary vasculature is an essential vessel network providing the blood supply to the heart ... of the developmental processes that underpin coronary vessel formation. From an ENU mutagenesis screen, we have isolated a mouse ...

    Abstract The coronary vasculature is an essential vessel network providing the blood supply to the heart. Disruptions in coronary blood flow contribute to cardiac disease, a major cause of premature death worldwide. The generation of treatments for cardiovascular disease will be aided by a deeper understanding of the developmental processes that underpin coronary vessel formation. From an ENU mutagenesis screen, we have isolated a mouse mutant displaying embryonic hydrocephalus and cardiac defects (EHC). Positional cloning and candidate gene analysis revealed that the EHC phenotype results from a point mutation in a splice donor site of the Myh10 gene, which encodes NMHC IIB. Complementation testing confirmed that the Myh10 mutation causes the EHC phenotype. Characterisation of the EHC cardiac defects revealed abnormalities in myocardial development, consistent with observations from previously generated NMHC IIB null mouse lines. Analysis of the EHC mutant hearts also identified defects in the formation of the coronary vasculature. We attribute the coronary vessel abnormalities to defective epicardial cell function, as the EHC epicardium displays an abnormal cell morphology, reduced capacity to undergo epithelial-mesenchymal transition (EMT), and impaired migration of epicardial-derived cells (EPDCs) into the myocardium. Our studies on the EHC mutant demonstrate a requirement for NMHC IIB in epicardial function and coronary vessel formation, highlighting the importance of this protein in cardiac development and ultimately, embryonic survival.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Coronary Vessels/growth & development ; Coronary Vessels/metabolism ; Embryo, Mammalian ; Embryonic Development/genetics ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Hydrocephalus/genetics ; Hydrocephalus/metabolism ; Hydrocephalus/pathology ; Mice ; Mice, Knockout ; Mutation ; Myocardium/metabolism ; Myosin Heavy Chains/genetics ; Nonmuscle Myosin Type IIB/genetics ; Pericardium/growth & development ; Pericardium/metabolism
    Chemical Substances Nonmuscle Myosin Type IIB (EC 3.6.1.-) ; nonmuscle myosin type IIB heavy chain (EC 3.6.1.-) ; Myosin Heavy Chains (EC 3.6.4.1)
    Language English
    Publishing date 2017-10-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1007068
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  10. Article ; Online: Spatial and temporal regulation of coronary vessel formation by calcineurin-NFAT signaling.

    Zeini, Miriam / Hang, Calvin T / Lehrer-Graiwer, Joshua / Dao, Tiffany / Zhou, Bin / Chang, Ching-Pin

    Development (Cambridge, England)

    2009  Volume 136, Issue 19, Page(s) 3335–3345

    Abstract: ... of calcineurin in either epicardial or myocardial cells had no effect on coronary vasculature during early ... Formation of the coronary vasculature requires reciprocal signaling between endothelial ... failed to develop normal coronary vasculature. To determine the cellular site at which calcineurin ...

    Abstract Formation of the coronary vasculature requires reciprocal signaling between endothelial, epicardially derived smooth muscle and underlying myocardial cells. Our studies show that calcineurin-NFAT signaling functions in endothelial cells within specific time windows to regulate coronary vessel development. Mouse embryos exposed to cyclosporin A (CsA), which inhibits calcineurin phosphatase activity, failed to develop normal coronary vasculature. To determine the cellular site at which calcineurin functions for coronary angiogenesis, we deleted calcineurin in endothelial, epicardial and myocardial cells. Disruption of calcineurin-NFAT signaling in endothelial cells resulted in the failure of coronary angiogenesis, recapitulating the coronary phenotype observed in CsA-treated embryos. By contrast, deletion of calcineurin in either epicardial or myocardial cells had no effect on coronary vasculature during early embryogenesis. To define the temporal requirement for NFAT signaling, we treated developing embryos with CsA at overlapping windows from E9.5 to E12.5 and examined coronary development at E12.5. These experiments demonstrated that calcineurin-NFAT signaling functions between E10.5 and E11.5 to regulate coronary angiogenesis. Consistent with these in vivo observations, endothelial cells exposed to CsA within specific time windows in tissue culture were unable to form tubular structures and their cellular responses to VEGF-A were blunted. Thus, our studies demonstrate specific temporal and spatial requirements of NFAT signaling for coronary vessel angiogenesis. These requirements are distinct from the roles of NFAT signaling in the angiogenesis of peripheral somatic vessels, providing an example of the environmental influence of different vascular beds on the in vivo endothelial responses to angiogenic stimuli.
    MeSH term(s) Animals ; Base Sequence ; Body Patterning ; Calcineurin/metabolism ; Calcineurin Inhibitors ; Cell Differentiation/drug effects ; Cells, Cultured ; Coronary Vessels/drug effects ; Coronary Vessels/embryology ; Coronary Vessels/metabolism ; Cyclosporine/pharmacology ; DNA Primers/genetics ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Humans ; In Vitro Techniques ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Cardiovascular ; NFATC Transcription Factors/metabolism ; Neovascularization, Physiologic/drug effects ; Signal Transduction
    Chemical Substances Calcineurin Inhibitors ; DNA Primers ; NFATC Transcription Factors ; Cyclosporine (83HN0GTJ6D) ; Calcineurin (EC 3.1.3.16)
    Language English
    Publishing date 2009-08-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.037903
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