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  1. Article ; Online: SARS-CoV-2: too infectious to handle?

    Coveney, Clarissa / Alderson, Jennifer

    Nature reviews. Immunology

    2020  Volume 20, Issue 8, Page(s) 462

    Keywords covid19
    Language English
    Publishing date 2020-06-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-020-0383-5
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  3. Article ; Online: SARS-CoV-2

    Coveney, Clarissa / Alderson, Jennifer

    Nature Reviews Immunology

    too infectious to handle?

    2020  Volume 20, Issue 8, Page(s) 462–462

    Keywords Immunology ; covid19
    Language English
    Publisher Springer Science and Business Media LLC
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-020-0383-5
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Techniques for Visualization and Quantification of Primary Cilia in Chondrocytes.

    Meng, Huan / Thompson, Clare L / Coveney, Clarissa R / Wann, Angus K / Knight, Martin M

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2598, Page(s) 157–176

    Abstract: Primary cilia regulate and coordinate a variety of cell signaling pathways important in chondrocyte physiology and cartilage development, health, and disease. Despite this, the chondrocyte primary cilium and its associated role in cartilage biology ... ...

    Abstract Primary cilia regulate and coordinate a variety of cell signaling pathways important in chondrocyte physiology and cartilage development, health, and disease. Despite this, the chondrocyte primary cilium and its associated role in cartilage biology remains poorly understood. Key to elucidating primary cilia structure and function in chondrocytes is the ability to visualize this unique structure. Here we describe materials and methods for immunofluorescence labeling, microscopy, and measurement of chondrocyte primary cilia.
    MeSH term(s) Chondrocytes/metabolism ; Cartilage, Articular/metabolism ; Cilia/metabolism ; Signal Transduction
    Language English
    Publishing date 2022-11-10
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2839-3_12
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  5. Article ; Online: Ciliary IFT88 Protects Coordinated Adolescent Growth Plate Ossification From Disruptive Physiological Mechanical Forces.

    Coveney, Clarissa R / Samvelyan, Hasmik J / Miotla-Zarebska, Jadwiga / Carnegie, Josephine / Chang, Emer / Corrin, C Jonty / Coveney, Trystan / Stott, Bryony / Parisi, Ida / Duarte, Claudia / Vincent, Tonia L / Staines, Katherine A / Wann, Angus Kt

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2022  Volume 37, Issue 6, Page(s) 1081–1096

    Abstract: Compared with our understanding of endochondral ossification, much less is known about the coordinated arrest of growth defined by the narrowing and fusion of the cartilaginous growth plate. Throughout the musculoskeletal system, appropriate cell and ... ...

    Abstract Compared with our understanding of endochondral ossification, much less is known about the coordinated arrest of growth defined by the narrowing and fusion of the cartilaginous growth plate. Throughout the musculoskeletal system, appropriate cell and tissue responses to mechanical force delineate morphogenesis and ensure lifelong health. It remains unclear how mechanical cues are integrated into many biological programs, including those coordinating the ossification of the adolescent growth plate at the cessation of growth. Primary cilia are microtubule-based organelles tuning a range of cell activities, including signaling cascades activated or modulated by extracellular biophysical cues. Cilia have been proposed to directly facilitate cell mechanotransduction. To explore the influence of primary cilia in the mouse adolescent limb, we conditionally targeted the ciliary gene Intraflagellar transport protein 88 (Ift88
    MeSH term(s) Animals ; Chondrocytes/metabolism ; Growth Plate/metabolism ; Hedgehog Proteins/metabolism ; Mechanotransduction, Cellular ; Mice ; Osteogenesis/physiology ; Tumor Suppressor Proteins/metabolism ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Hedgehog Proteins ; Tg737Rpw protein, mouse ; Tumor Suppressor Proteins ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2022-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.4502
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  6. Article ; Online: Role of Ciliary Protein Intraflagellar Transport Protein 88 in the Regulation of Cartilage Thickness and Osteoarthritis Development in Mice.

    Coveney, Clarissa R / Zhu, Linyi / Miotla-Zarebska, Jadwiga / Stott, Bryony / Parisi, Ida / Batchelor, Vicky / Duarte, Claudia / Chang, Emer / McSorley, Eleanor / Vincent, Tonia L / Wann, Angus K T

    Arthritis & rheumatology (Hoboken, N.J.)

    2021  Volume 74, Issue 1, Page(s) 49–59

    Abstract: Objective: Mechanical and biologic cues drive cellular signaling in cartilage development, health, and disease. Primary cilia proteins, which are implicated in the transduction of biologic and physiochemical signals, control cartilage formation during ... ...

    Abstract Objective: Mechanical and biologic cues drive cellular signaling in cartilage development, health, and disease. Primary cilia proteins, which are implicated in the transduction of biologic and physiochemical signals, control cartilage formation during skeletal development. This study was undertaken to assess the influence of the ciliary protein intraflagellar transport protein 88 (IFT88) on postnatal cartilage from mice with conditional knockout of the Ift88 gene (Ift88-KO).
    Methods: Ift88
    Results: Deletion of Ift88 resulted in progressive reduction in the thickness of the medial tibial cartilage in adolescent mice, as well as marked atrophy of the cartilage in mice during adulthood. In aggrecanCre
    Conclusion: Our results in a mouse model of OA demonstrate that IFT88 performs a chondroprotective role in articular cartilage by controlling the calcification of cartilage via maintenance of a threshold of Hh signaling during physiologic loading.
    MeSH term(s) Animals ; Cartilage, Articular/anatomy & histology ; Cartilage, Articular/growth & development ; Male ; Mice ; Mice, Knockout ; Organ Size ; Osteoarthritis/etiology ; Tumor Suppressor Proteins/physiology
    Chemical Substances Tg737Rpw protein, mouse ; Tumor Suppressor Proteins
    Language English
    Publishing date 2021-12-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41894
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  7. Article ; Online: Ciliary proteins specify the cell inflammatory response by tuning NFκB signalling, independently of primary cilia.

    Mc Fie, Megan / Koneva, Lada / Collins, Isabella / Coveney, Clarissa R / Clube, Aisling M / Chanalaris, Anastasios / Vincent, Tonia L / Bezbradica, Jelena S / Sansom, Stephen N / Wann, Angus K T

    Journal of cell science

    2020  Volume 133, Issue 13

    Abstract: Complex inflammatory signalling cascades define the response to tissue injury but also control development and homeostasis, limiting the potential for these pathways to be targeted therapeutically. Primary cilia are subcellular regulators of cellular ... ...

    Abstract Complex inflammatory signalling cascades define the response to tissue injury but also control development and homeostasis, limiting the potential for these pathways to be targeted therapeutically. Primary cilia are subcellular regulators of cellular signalling, controlling how signalling is organized, encoded and, in some instances, driving or influencing pathogenesis. Our previous research revealed that disruption of ciliary intraflagellar transport (IFT), altered the cell response to IL-1β, supporting a putative link emerging between cilia and inflammation. Here, we show that IFT88 depletion affects specific cytokine-regulated behaviours, changing cytosolic NFκB translocation dynamics but leaving MAPK signalling unaffected. RNA-seq analysis indicates that IFT88 regulates one third of the genome-wide targets, including the pro-inflammatory genes
    MeSH term(s) Cilia/metabolism ; Flagella/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Protein Transport ; Signal Transduction
    Chemical Substances NF-kappa B
    Language English
    Publishing date 2020-07-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.239871
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  8. Article ; Online: Innate immunology in COVID-19-a living review. Part II: dysregulated inflammation drives immunopathology.

    Rodrigues, Patrícia R S / Alrubayyi, Aljawharah / Pring, Ellie / Bart, Valentina M T / Jones, Ruth / Coveney, Clarissa / Lu, Fangfang / Tellier, Michael / Maleki-Toyserkani, Shayda / Richter, Felix C / Scourfield, D Oliver / Gea-Mallorquí, Ester / Davies, Luke C

    Oxford open immunology

    2020  Volume 1, Issue 1, Page(s) iqaa005

    Abstract: The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate ...

    Abstract The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1β-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19.
    Language English
    Publishing date 2020-12-08
    Publishing country England
    Document type Journal Article
    ISSN 2633-6960
    ISSN (online) 2633-6960
    DOI 10.1093/oxfimm/iqaa005
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  9. Article ; Online: Cilia protein IFT88 regulates extracellular protease activity by optimizing LRP-1-mediated endocytosis.

    Coveney, Clarissa R / Collins, Isabella / Mc Fie, Megan / Chanalaris, Anastasios / Yamamoto, Kazuhiro / Wann, Angus K T

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2018  , Page(s) fj201800334

    Abstract: ... in matrix turnover and LRP-1 function, with potential relevance in a range of diseases.-Coveney, C. R ...

    Abstract Matrix protease activity is fundamental to developmental tissue patterning and remains influential in adult homeostasis. In cartilage, the principal matrix proteoglycan is aggrecan, the protease-mediated catabolism of which defines arthritis; however, the pathophysiologic mechanisms that drive aberrant aggrecanolytic activity remain unclear. Human ciliopathies exhibit altered matrix, which has been proposed to be the result of dysregulated hedgehog signaling that is tuned within the primary cilium. Here, we report that disruption of intraflagellar transport protein 88 (IFT88), a core ciliary trafficking protein, increases chondrocyte aggrecanase activity in vitro. We find that the receptor for protease endocytosis in chondrocytes, LDL receptor-related protein 1 (LRP-1), is unevenly distributed over the cell membrane, often concentrated at the site of cilia assembly. Hypomorphic mutation of IFT88 disturbs this apparent hot spot for protease uptake, increases receptor shedding, and results in a reduced rate of protease clearance from the extracellular space. We propose that IFT88 and/or the cilium regulates the extracellular remodeling of matrix-independently of Hedgehog regulation-by enabling rapid LRP-1-mediated endocytosis of proteases, potentially by supporting the creation of a ciliary pocket. This result highlights new roles for the cilium's machinery in matrix turnover and LRP-1 function, with potential relevance in a range of diseases.-Coveney, C. R., Collins, I., Mc Fie, M., Chanalaris, A., Yamamoto, K., Wann, A. K. T. Cilia protein IFT88 regulates extracellular protease activity by optimizing LRP-1-mediated endocytosis.
    Language English
    Publishing date 2018-06-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201800334
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  10. Article ; Online: Innate immunology in COVID-19-a living review. Part I: viral entry, sensing and evasion.

    Coveney, Clarissa / Tellier, Michel / Lu, Fangfang / Maleki-Toyserkani, Shayda / Jones, Ruth / Bart, Valentina M T / Pring, Ellie / Alrubayyi, Aljawharah / Richter, Felix C / Scourfield, D Oliver / Rehwinkel, Jan / Rodrigues, Patrícia R S / Davies, Luke C / Gea-Mallorquí, Ester

    Oxford open immunology

    2020  Volume 1, Issue 1, Page(s) iqaa004

    Abstract: The coronavirus infectious disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a world health concern and can cause severe disease and high mortality in susceptible groups. While vaccines offer ... ...

    Abstract The coronavirus infectious disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a world health concern and can cause severe disease and high mortality in susceptible groups. While vaccines offer a chance to treat disease, prophylactic and anti-viral treatments are still of vital importance, especially in context of the mutative ability of this group of viruses. Therefore, it is essential to elucidate the molecular mechanisms of viral entry, innate sensing and immune evasion of SARS-CoV-2, which control the triggers of the subsequent excessive inflammatory response. Viral evasion strategies directly target anti-viral immunity, counteracting host restriction factors and hijacking signalling pathways to interfere with interferon production. In Part I of this review, we examine SARS-CoV-2 viral entry and the described immune evasion mechanisms to provide a perspective on how the failure in initial viral sensing by infected cells can lead to immune dysregulation causing fatal COVID-19, discussed in Part II.
    Language English
    Publishing date 2020-12-08
    Publishing country England
    Document type Journal Article
    ISSN 2633-6960
    ISSN (online) 2633-6960
    DOI 10.1093/oxfimm/iqaa004
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