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  1. Article ; Online: Vascular underpinning of COVID-19.

    Wazny, Vanessa / Siau, Anthony / Wu, Kan Xing / Cheung, Christine

    Open biology

    2020  Volume 10, Issue 8, Page(s) 200208

    Abstract: COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, ...

    Abstract COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication. Finally, we provide experimental considerations such as endothelial polarity, cellular heterogeneity in organoids and shear stress dynamics in designing cellular models to facilitate research on viral-induced endothelial dysfunctions. Understanding the vascular underpinning of COVID-19 pathogenesis is crucial to managing outcomes and mortality.
    MeSH term(s) Angiotensin-Converting Enzyme 2 ; Betacoronavirus/metabolism ; COVID-19 ; Capillary Permeability/physiology ; Comorbidity ; Coronavirus Infections/immunology ; Coronavirus Infections/mortality ; Coronavirus Infections/pathology ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/pathology ; Cytokines/blood ; Endothelial Cells/pathology ; Endothelial Cells/virology ; Humans ; Inflammation/pathology ; Pandemics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/immunology ; Pneumonia, Viral/mortality ; Pneumonia, Viral/pathology ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/pathology ; SARS-CoV-2 ; Severity of Illness Index ; Thrombosis/pathology ; Virus Internalization
    Chemical Substances Cytokines ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Keywords covid19
    Language English
    Publishing date 2020-08-27
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2630944-0
    ISSN 2046-2441 ; 2046-2441
    ISSN (online) 2046-2441
    ISSN 2046-2441
    DOI 10.1098/rsob.200208
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Single-Cell Transcriptome of Wet AMD Patient-Derived Endothelial Cells in Angiogenic Sprouting.

    Yeo, Natalie Jia Ying / Wazny, Vanessa / Nguyen, Nhi Le Uyen / Ng, Chun-Yi / Wu, Kan Xing / Fan, Qiao / Cheung, Chui Ming Gemmy / Cheung, Christine

    International journal of molecular sciences

    2022  Volume 23, Issue 20

    Abstract: Age-related macular degeneration (AMD) is a global leading cause of visual impairment in older populations. 'Wet' AMD, the most common subtype of this disease, occurs when pathological angiogenesis infiltrates the subretinal space (choroidal ... ...

    Abstract Age-related macular degeneration (AMD) is a global leading cause of visual impairment in older populations. 'Wet' AMD, the most common subtype of this disease, occurs when pathological angiogenesis infiltrates the subretinal space (choroidal neovascularization), causing hemorrhage and retinal damage. Gold standard anti-vascular endothelial growth factor (VEGF) treatment is an effective therapy, but the long-term prevention of visual decline has not been as successful. This warrants the need to elucidate potential VEGF-independent pathways. We generated blood out-growth endothelial cells (BOECs) from wet AMD and normal control subjects, then induced angiogenic sprouting of BOECs using a fibrin gel bead assay. To deconvolute endothelial heterogeneity, we performed single-cell transcriptomic analysis on the sprouting BOECs, revealing a spectrum of cell states. Our wet AMD BOECs share common pathways with choroidal neovascularization such as extracellular matrix remodeling that promoted proangiogenic phenotype, and our 'activated' BOEC subpopulation demonstrated proinflammatory hallmarks, resembling the tip-like cells in vivo. We uncovered new molecular insights that pathological angiogenesis in wet AMD BOECs could also be driven by interleukin signaling and amino acid metabolism. A web-based visualization of the sprouting BOEC single-cell transcriptome has been created to facilitate further discovery research.
    MeSH term(s) Humans ; Choroidal Neovascularization/drug therapy ; Transcriptome ; Vascular Endothelial Growth Factor A/metabolism ; Endothelial Cells/metabolism ; Wet Macular Degeneration/drug therapy ; Vascular Endothelial Growth Factors ; Interleukins/therapeutic use ; Amino Acids ; Fibrin ; Angiogenesis Inhibitors/therapeutic use
    Chemical Substances Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Interleukins ; Amino Acids ; Fibrin (9001-31-4) ; Angiogenesis Inhibitors
    Language English
    Publishing date 2022-10-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms232012549
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Vascular underpinning of COVID-19

    Vanessa Wazny / Anthony Siau / Kan Xing Wu / Christine Cheung

    Open Biology, Vol 10, Iss

    2020  Volume 8

    Abstract: COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, ...

    Abstract COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication. Finally, we provide experimental considerations such as endothelial polarity, cellular heterogeneity in organoids and shear stress dynamics in designing cellular models to facilitate research on viral-induced endothelial dysfunctions. Understanding the vascular underpinning of COVID-19 pathogenesis is crucial to managing outcomes and mortality.
    Keywords endothelial dysfunction ; virus ; vascular biology ; Biology (General) ; QH301-705.5 ; covid19
    Subject code 570
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher The Royal Society
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Vascular underpinning of COVID-19

    Wazny, Vanessa / Siau, Anthony / Wu, Kan Xing / Cheung, Christine

    Open Biol

    Abstract: COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, ...

    Abstract COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication. Finally, we provide experimental considerations such as endothelial polarity, cellular heterogeneity in organoids and shear stress dynamics in designing cellular models to facilitate research on viral-induced endothelial dysfunctions. Understanding the vascular underpinning of COVID-19 pathogenesis is crucial to managing outcomes and mortality.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #733298
    Database COVID19

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  5. Article ; Online: Vascular underpinning of COVID-19

    Wazny, Vanessa / Siau, Anthony / Wu, Kan Xing / Cheung, Christine

    Open Biology

    2020  Volume 10, Issue 8, Page(s) 200208

    Abstract: COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, ...

    Abstract COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication. Finally, we provide experimental considerations such as endothelial polarity, cellular heterogeneity in organoids and shear stress dynamics in designing cellular models to facilitate research on viral-induced endothelial dysfunctions. Understanding the vascular underpinning of COVID-19 pathogenesis is crucial to managing outcomes and mortality.
    Keywords covid19
    Language English
    Publisher The Royal Society
    Publishing country uk
    Document type Article ; Online
    ZDB-ID 2630944-0
    ISSN 2046-2441
    ISSN 2046-2441
    DOI 10.1098/rsob.200208
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  6. Article ; Online: A Human Pleiotropic Multiorgan Condition Caused by Deficient Wnt Secretion.

    Chai, Guoliang / Szenker-Ravi, Emmanuelle / Chung, Changuk / Li, Zhen / Wang, Lu / Khatoo, Muznah / Marshall, Trevor / Jiang, Nan / Yang, Xiaoxu / McEvoy-Venneri, Jennifer / Stanley, Valentina / Anzenberg, Paula / Lang, Nhi / Wazny, Vanessa / Yu, Jia / Virshup, David M / Nygaard, Rie / Mancia, Filippo / Merdzanic, Rijad /
    Toralles, Maria B P / Pitanga, Paula M L / Puri, Ratna D / Hernan, Rebecca / Chung, Wendy K / Bertoli-Avella, Aida M / Al-Sannaa, Nouriya / Zaki, Maha S / Willert, Karl / Reversade, Bruno / Gleeson, Joseph G

    The New England journal of medicine

    2021  Volume 385, Issue 14, Page(s) 1292–1301

    Abstract: Background: Structural birth defects occur in approximately 3% of live births; most such defects lack defined genetic or environmental causes. Despite advances in surgical approaches, pharmacologic prevention remains largely out of reach.: Methods: ... ...

    Abstract Background: Structural birth defects occur in approximately 3% of live births; most such defects lack defined genetic or environmental causes. Despite advances in surgical approaches, pharmacologic prevention remains largely out of reach.
    Methods: We queried worldwide databases of 20,248 families that included children with neurodevelopmental disorders and that were enriched for parental consanguinity. Approximately one third of affected children in these families presented with structural birth defects or microcephaly. We performed exome or genome sequencing of samples obtained from the children, their parents, or both to identify genes with biallelic pathogenic or likely pathogenic mutations present in more than one family. After identifying disease-causing variants, we generated two mouse models, each with a pathogenic variant "knocked in," to study mechanisms and test candidate treatments. We administered a small-molecule Wnt agonist to pregnant animals and assessed their offspring.
    Results: We identified homozygous mutations in
    Conclusions: Genetic variations affecting a central Wnt regulator caused syndromic structural birth defects. Results from mouse models suggest that what we have named Zaki syndrome is a potentially preventable disorder. (Funded by the National Institutes of Health and others.).
    MeSH term(s) Abnormalities, Multiple/genetics ; Animals ; Congenital Abnormalities/genetics ; Disease Models, Animal ; Fibroblasts/metabolism ; Gene Knock-In Techniques ; Genes, Recessive ; Genetic Pleiotropy ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Transgenic ; Mutation ; Pedigree ; Phenotype ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Syndrome ; Wnt Proteins/metabolism ; Wnt Signaling Pathway
    Chemical Substances Gpr177 protein, mouse ; Intracellular Signaling Peptides and Proteins ; Receptors, G-Protein-Coupled ; WLS protein, human ; Wnt Proteins
    Language English
    Publishing date 2021-09-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMoa2033911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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