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  1. Article ; Online: Opening the vascular gate.

    Malinova, Tsveta S / Huveneers, Stephan

    Nature nanotechnology

    2019  Volume 14, Issue 3, Page(s) 195–196

    MeSH term(s) Breast Neoplasms ; Humans ; Ion Channel Gating ; Models, Molecular ; Nanoparticles
    Language English
    Publishing date 2019-01-28
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2254964-X
    ISSN 1748-3395 ; 1748-3387
    ISSN (online) 1748-3395
    ISSN 1748-3387
    DOI 10.1038/s41565-019-0372-7
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  2. Article ; Online: Sensing of Cytoskeletal Forces by Asymmetric Adherens Junctions.

    Malinova, Tsveta S / Huveneers, Stephan

    Trends in cell biology

    2017  Volume 28, Issue 4, Page(s) 328–341

    Abstract: Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked ... ...

    Abstract Within tissues, key cellular adaptations occur via mechanotransduction responses at cell-cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell-cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell-cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease.
    MeSH term(s) Actomyosin/metabolism ; Adherens Junctions/metabolism ; Animals ; Cadherins/metabolism ; Cell Membrane/metabolism ; Cytoskeleton/metabolism ; Endocytosis/physiology ; Humans ; Mechanotransduction, Cellular/physiology ; Models, Biological
    Chemical Substances Cadherins ; Actomyosin (9013-26-7)
    Language English
    Publishing date 2017-11-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2017.11.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Jg. 1995 - 2021: Lesesall (2.OG)
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  3. Article ; Online: Serotonin: A mediator of the gut-brain axis in multiple sclerosis.

    Malinova, Tsveta S / Dijkstra, Christine D / de Vries, Helga E

    Multiple sclerosis (Houndmills, Basingstoke, England)

    2017  Volume 24, Issue 9, Page(s) 1144–1150

    Abstract: Background: The significance of the gut microbiome for the pathogenesis of multiple sclerosis (MS) has been established, although the underlying signaling mechanisms of this interaction have not been sufficiently explored.: Objectives: We address ... ...

    Abstract Background: The significance of the gut microbiome for the pathogenesis of multiple sclerosis (MS) has been established, although the underlying signaling mechanisms of this interaction have not been sufficiently explored.
    Objectives: We address this point and use serotonin (5-hydroxytryptamine (5-HT))-a microbial-modulated neurotransmitter (NT) as a showcase to demonstrate that NTs regulated by the gut microbiome are potent candidates for mediators of the gut-brain axis in demyelinating disorders. Methods, Results, and Conclusion: Our comprehensive overview of literature provides evidence that 5-HT levels in the gut are controlled by the microbiome, both via secretion and through regulation of metabolites. In addition, we demonstrate that the gut microbiome can influence the formation of the serotonergic system (SS) in the brain. We also show that SS alterations have been related to MS directly-altered expression of 5-HT transporters in central nervous system (CNS) and indirectly-beneficial effects of 5-HT modulating drugs on the course of the disease and higher prevalence of depression in patients with MS. Finally, we discuss briefly the role of other microbiome-modulated NTs such as γ-aminobutyric acid and dopamine in MS to highlight a new direction for future research aiming to relate microbiome-regulated NTs to demyelinating disorders.
    MeSH term(s) Animals ; Gastrointestinal Microbiome/immunology ; Humans ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/microbiology ; Neuroimmunomodulation/physiology ; Serotonin/metabolism
    Chemical Substances Serotonin (333DO1RDJY)
    Language English
    Publishing date 2017-11-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1290669-4
    ISSN 1477-0970 ; 1352-4585
    ISSN (online) 1477-0970
    ISSN 1352-4585
    DOI 10.1177/1352458517739975
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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis.

    Malinova, Tsveta S / Angulo-Urarte, Ana / Nüchel, Julian / Tauber, Marina / van der Stoel, Miesje M / Janssen, Vera / de Haan, Annett / Groenen, Anouk G / Tebbens, Merel / Graupera, Mariona / Plomann, Markus / Huveneers, Stephan

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 2610

    Abstract: Angiogenic sprouting relies on collective migration and coordinated rearrangements of endothelial leader and follower cells. VE-cadherin-based adherens junctions have emerged as key cell-cell contacts that transmit forces between cells and trigger ... ...

    Abstract Angiogenic sprouting relies on collective migration and coordinated rearrangements of endothelial leader and follower cells. VE-cadherin-based adherens junctions have emerged as key cell-cell contacts that transmit forces between cells and trigger signals during collective cell migration in angiogenesis. However, the underlying molecular mechanisms that govern these processes and their functional importance for vascular development still remain unknown. We previously showed that the F-BAR protein PACSIN2 is recruited to tensile asymmetric adherens junctions between leader and follower cells. Here we report that PACSIN2 mediates the formation of endothelial sprouts during angiogenesis by coordinating collective migration. We show that PACSIN2 recruits the trafficking regulators EHD4 and MICAL-L1 to the rear end of asymmetric adherens junctions to form a recycling endosome-like tubular structure. The junctional PACSIN2/EHD4/MICAL-L1 complex controls local VE-cadherin trafficking and thereby coordinates polarized endothelial migration and angiogenesis. Our findings reveal a molecular event at force-dependent asymmetric adherens junctions that occurs during the tug-of-war between endothelial leader and follower cells, and allows for junction-based guidance during collective migration in angiogenesis.
    Language English
    Publishing date 2021-05-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-22873-y
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  5. Article ; Online: Diverse ultrastructural landscape of atherosclerotic endothelium.

    Kluza, Ewelina / Beldman, Thijs J / Shami, Annelie / Scholl, Edwin R / Malinova, Tsveta S / Grootemaat, Anita E / van der Wel, Nicole N / Gonçalves, Isabel / Huveneers, Stephan / Mulder, Willem J M / Lutgens, Esther

    Atherosclerosis

    2021  Volume 339, Page(s) 35–45

    Abstract: Background and aims: The endothelium plays a major role in atherosclerosis, yet the endothelial plaque surface is a largely uncharted territory. Here we hypothesize that atherosclerosis-driven remodeling of the endothelium is a dynamic process, ... ...

    Abstract Background and aims: The endothelium plays a major role in atherosclerosis, yet the endothelial plaque surface is a largely uncharted territory. Here we hypothesize that atherosclerosis-driven remodeling of the endothelium is a dynamic process, involving both damaging and regenerative mechanisms.
    Methods: Using scanning electron microscopy (SEM) and immuno-SEM, we studied endothelial junction ultrastructure, endothelial openings and immune cell-endothelium interactions in eight apoe
    Results: The surface of early mouse plaques (n = 11) displayed a broad range of morphological alterations, including junctional disruptions and large transcellular endothelial pores with the average diameter between 0.6 and 3 μm. The shoulder region of advanced atherosclerotic lesions (n = 7) had a more aggravated morphology with 8 μm-size paracellular openings at two-fold higher density. In contrast, the central apical surface of advanced plaques, i.e., the plaque body (n = 7), displayed endothelial normalization, as shown by a significantly higher frequency of intact endothelial junctions and a lower incidence of paracellular pores. This normalized endothelial phenotype correlated with low immune cell density (only 5 cells/mm
    Conclusions: Our study unveils the spectrum of endothelial abnormalities associated with the development of atherosclerosis. These were highly abundant in early lesions and in the shoulder region of advanced plaques, while normalized at the advanced plaque's body. Similar endothelial features were observed in human atherosclerotic plaques, underlining the versatility of endothelial transformations in atherosclerosis.
    MeSH term(s) Animals ; Atherosclerosis ; Carotid Arteries ; Endothelium ; Mice ; Microscopy, Electron, Scanning ; Plaque, Atherosclerotic
    Language English
    Publishing date 2021-11-19
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2021.11.017
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 226: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Nanoparticle-Aided Characterization of Arterial Endothelial Architecture during Atherosclerosis Progression and Metabolic Therapy.

    Beldman, Thijs J / Malinova, Tsveta S / Desclos, Emilie / Grootemaat, Anita E / Misiak, Aresh L S / van der Velden, Saskia / van Roomen, Cindy P A A / Beckers, Linda / van Veen, Henk A / Krawczyk, Przemyslaw M / Hoebe, Ron A / Sluimer, Judith C / Neele, Annette E / de Winther, Menno P J / van der Wel, Nicole N / Lutgens, Esther / Mulder, Willem J M / Huveneers, Stephan / Kluza, Ewelina

    ACS nano

    2019  Volume 13, Issue 12, Page(s) 13759–13774

    Abstract: Atherosclerosis is associated with a compromised endothelial barrier, facilitating the accumulation of immune cells and macromolecules in atherosclerotic lesions. In this study, we investigate endothelial barrier integrity and the enhanced permeability ... ...

    Abstract Atherosclerosis is associated with a compromised endothelial barrier, facilitating the accumulation of immune cells and macromolecules in atherosclerotic lesions. In this study, we investigate endothelial barrier integrity and the enhanced permeability and retention (EPR) effect during atherosclerosis progression and therapy in
    MeSH term(s) Animals ; Arteries/pathology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/therapy ; Disease Progression ; Endothelium, Vascular/pathology ; Entropy ; Europium/chemistry ; Mice ; Nanoparticles/chemistry ; Probability ; Temperature
    Chemical Substances Europium (444W947O8O)
    Language English
    Publishing date 2019-07-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1936-086X
    ISSN (online) 1936-086X
    DOI 10.1021/acsnano.8b08875
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  7. Article ; Online: The F-BAR protein pacsin2 inhibits asymmetric VE-cadherin internalization from tensile adherens junctions.

    Dorland, Yvonne L / Malinova, Tsveta S / van Stalborch, Anne-Marieke D / Grieve, Adam G / van Geemen, Daphne / Jansen, Nicolette S / de Kreuk, Bart-Jan / Nawaz, Kalim / Kole, Jeroen / Geerts, Dirk / Musters, René J P / de Rooij, Johan / Hordijk, Peter L / Huveneers, Stephan

    Nature communications

    2016  Volume 7, Page(s) 12210

    Abstract: Vascular homoeostasis, development and disease critically depend on the regulation of endothelial cell-cell junctions. Here we uncover a new role for the F-BAR protein pacsin2 in the control of VE-cadherin-based endothelial adhesion. Pacsin2 concentrates ...

    Abstract Vascular homoeostasis, development and disease critically depend on the regulation of endothelial cell-cell junctions. Here we uncover a new role for the F-BAR protein pacsin2 in the control of VE-cadherin-based endothelial adhesion. Pacsin2 concentrates at focal adherens junctions (FAJs) that are experiencing unbalanced actomyosin-based pulling. FAJs move in response to differences in local cytoskeletal geometry and pacsin2 is recruited consistently to the trailing end of fast-moving FAJs via a mechanism that requires an intact F-BAR domain. Photoconversion, photobleaching, immunofluorescence and super-resolution microscopy reveal polarized dynamics, and organization of junctional proteins between the front of FAJs and their trailing ends. Interestingly, pacsin2 recruitment inhibits internalization of the VE-cadherin complex from FAJ trailing ends and is important for endothelial monolayer integrity. Together, these findings reveal a novel junction protective mechanism during polarized trafficking of VE-cadherin, which supports barrier maintenance within dynamic endothelial tissue.
    MeSH term(s) Actomyosin/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Adherens Junctions/metabolism ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Cadherins/genetics ; Cadherins/metabolism ; Focal Adhesions/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Microscopy, Fluorescence/methods
    Chemical Substances Adaptor Proteins, Signal Transducing ; Antigens, CD ; Cadherins ; PACSIN2 protein, human ; cadherin 5 ; Actomyosin (9013-26-7)
    Language English
    Publishing date 2016-07-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/ncomms12210
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