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  1. Artikel ; Online: The senescent secretome drives PLVAP expression in cultured human hepatic endothelial cells to promote monocyte transmigration

    Alex L. Wilkinson / Samuel Hulme / James I. Kennedy / Emily R. Mann / Paul Horn / Emma L. Shepherd / Kelvin Yin / Marco Y.W. Zaki / Gareth Hardisty / Wei-Yu Lu / Pia Rantakari / David H. Adams / Marko Salmi / Matthew Hoare / Daniel A. Patten / Shishir Shetty

    iScience, Vol 26, Iss 10, Pp 107966- (2023)

    2023  

    Abstract: Summary: Liver sinusoidal endothelial cells (LSEC) undergo significant phenotypic change in chronic liver disease (CLD), and yet the factors that drive this process and the impact on their function as a vascular barrier and gatekeeper for immune cell ... ...

    Abstract Summary: Liver sinusoidal endothelial cells (LSEC) undergo significant phenotypic change in chronic liver disease (CLD), and yet the factors that drive this process and the impact on their function as a vascular barrier and gatekeeper for immune cell recruitment are poorly understood. Plasmalemma-vesicle-associated protein (PLVAP) has been characterized as a marker of LSEC in CLD; notably we found that PLVAP upregulation strongly correlated with markers of tissue senescence. Furthermore, exposure of human LSEC to the senescence-associated secretory phenotype (SASP) led to a significant upregulation of PLVAP. Flow-based assays demonstrated that SASP-driven leukocyte recruitment was characterized by paracellular transmigration of monocytes while the majority of lymphocytes migrated transcellularly. Knockdown studies confirmed that PLVAP selectively supported monocyte transmigration mediated through PLVAP’s impact on LSEC permeability by regulating phospho-VE-cadherin expression and endothelial gap formation. PLVAP may therefore represent an endothelial target that selectively shapes the senescence-mediated immune microenvironment in liver disease.
    Schlagwörter Microenvironment ; Molecular biology ; Cell biology ; Omics ; Transcriptomics ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-10-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure

    Abhishek Chauhan / Lozan Sheriff / Mohammed T. Hussain / Gwilym J. Webb / Daniel A. Patten / Emma L. Shepherd / Robert Shaw / Christopher J. Weston / Debashis Haldar / Samuel Bourke / Rajan Bhandari / Stephanie Watson / David H. Adams / Steve P. Watson / Patricia F. Lalor

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 12

    Abstract: The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute ...

    Abstract The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute liver injury by blocking restorative neutrophil driven inflammation.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-04-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: The platelet receptor CLEC-2 blocks neutrophil mediated hepatic recovery in acetaminophen induced acute liver failure

    Abhishek Chauhan / Lozan Sheriff / Mohammed T. Hussain / Gwilym J. Webb / Daniel A. Patten / Emma L. Shepherd / Robert Shaw / Christopher J. Weston / Debashis Haldar / Samuel Bourke / Rajan Bhandari / Stephanie Watson / David H. Adams / Steve P. Watson / Patricia F. Lalor

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 12

    Abstract: The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute ...

    Abstract The molecular mechanisms that drive irreversible acute liver failure remain poorly characterized. Here, the authors show that the recently discovered platelet receptor CLEC-2 (C-type lectin-like receptor) perpetuates and worsens liver damage during acute liver injury by blocking restorative neutrophil driven inflammation.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-04-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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