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  1. AU="Bagley, Dustin C"
  2. AU="Van der Linden, Nicolas"
  3. AU=Cammarota Giovanni
  4. AU=Aziz Arif
  5. AU="Ormandy, Judy"
  6. AU="Akgun, B"
  7. AU="Sang Yup Lee"
  8. AU=Ahuja Preeti
  9. AU=Zulhendri Felix
  10. AU=Suhail Shanzay
  11. AU="Masum, Hassan"
  12. AU="Del Águila, Javier García"
  13. AU="Balian, Dikran Raffi"
  14. AU="Starr, Megan M"
  15. AU=Rajapaksa Shabna
  16. AU="Mohammed Aly Abdou" AU="Mohammed Aly Abdou"
  17. AU=Cooper Isabella D
  18. AU="Luis Rivera-Armenta, Jose"
  19. AU="Zahid Shaikh"
  20. AU="Scovil, Carol"
  21. AU="Grove, Nico"
  22. AU="McGuire, K J"
  23. AU="Martin, Bianca Aparecida"
  24. AU="Hampton, Joshua Trae"
  25. AU=Thesen Thomas
  26. AU=Oliveira Giuliano da Paz
  27. AU="García, Patricia J"
  28. AU="Hosseinpanah, Farhad"
  29. AU="Mayuni, Grace"
  30. AU="Volkova, Yulia L"
  31. AU="Dauwerse, Sierk"

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Treffer 1 - 7 von insgesamt 7

Suchoptionen

  1. Artikel: The epithelium takes the stage in asthma and inflammatory bowel diseases.

    López-Posadas, Rocío / Bagley, Dustin C / Pardo-Pastor, Carlos / Ortiz-Zapater, Elena

    Frontiers in cell and developmental biology

    2024  Band 12, Seite(n) 1258859

    Abstract: The epithelium is a dynamic barrier and the damage to this epithelial layer governs a variety of complex mechanisms involving not only epithelial cells but all resident tissue constituents, including immune and stroma cells. Traditionally, diseases ... ...

    Abstract The epithelium is a dynamic barrier and the damage to this epithelial layer governs a variety of complex mechanisms involving not only epithelial cells but all resident tissue constituents, including immune and stroma cells. Traditionally, diseases characterized by a damaged epithelium have been considered "immunological diseases," and research efforts aimed at preventing and treating these diseases have primarily focused on immuno-centric therapeutic strategies, that often fail to halt or reverse the natural progression of the disease. In this review, we intend to focus on specific mechanisms driven by the epithelium that ensure barrier function. We will bring asthma and Inflammatory Bowel Diseases into the spotlight, as we believe that these two diseases serve as pertinent examples of epithelium derived pathologies. Finally, we will argue how targeting the epithelium is emerging as a novel therapeutic strategy that holds promise for addressing these chronic diseases.
    Sprache Englisch
    Erscheinungsdatum 2024-03-11
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2024.1258859
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Mon1a and FCHO2 are required for maintenance of Golgi architecture.

    Bagley, Dustin C / Morham, Scott G / Kaplan, Jerry / Ward, Diane M

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Mon1a has been shown to function in the endolysosomal pathway functioning in the Mon1-Ccz1 complex and it also acts in the secretory pathway where it interacts with dynein and affects ER to Golgi traffic. Here we show that Mon1a is also required for ... ...

    Abstract Mon1a has been shown to function in the endolysosomal pathway functioning in the Mon1-Ccz1 complex and it also acts in the secretory pathway where it interacts with dynein and affects ER to Golgi traffic. Here we show that Mon1a is also required for maintenance of the Golgi apparatus. We identified the F-BAR protein FCHO2 as a Mon1a-interacting protein by both yeast two-hybrid analysis and co-immunoprecipitation. siRNA-dependent reductions in Mon1a or FCHO2 resulted in Golgi fragmentation. Membrane trafficking through the secretory apparatus in FCHO2-depleted cells was unaltered, however, reduction of FCHO2 affected the uniform distribution of Golgi enzymes necessary for carbohydrate modification. Fluorescence recovery after photobleaching analysis showed that the Golgi ministacks in Mon1a- or FCHO2-silenced cells did not exchange resident membrane proteins. The effect of FCHO2 silencing on Golgi structure was partially cell cycle-dependent and required mitosis-dependent Golgi fragmentation, whereas the effect of Mon1a-silencing on Golgi disruption was not cell cycle-dependent. mCherry-FCHO2 transiently colocalized on Golgi structures independent of Mon1a. These findings suggest that Mon1a has functions throughout the secretory pathway including interacting with dynein at the ER-Golgi interface in vesicle formation and then interacting with FCHO2 at the Golgi to generate lateral links between ministacks, thus creating Golgi ribbons.
    Sprache Englisch
    Erscheinungsdatum 2023-07-07
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.07.06.547837
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Bronchoconstriction damages airway epithelia by crowding-induced excess cell extrusion.

    Bagley, Dustin C / Russell, Tobias / Ortiz-Zapater, Elena / Stinson, Sally / Fox, Kristina / Redd, Polly F / Joseph, Merry / Deering-Rice, Cassandra / Reilly, Christopher / Parsons, Maddy / Brightling, Christopher / Rosenblatt, Jody

    Science (New York, N.Y.)

    2024  Band 384, Heft 6691, Seite(n) 66–73

    Abstract: Asthma is deemed an inflammatory disease, yet the defining diagnostic feature is mechanical bronchoconstriction. We previously discovered a conserved process called cell extrusion that drives homeostatic epithelial cell death when cells become too ... ...

    Abstract Asthma is deemed an inflammatory disease, yet the defining diagnostic feature is mechanical bronchoconstriction. We previously discovered a conserved process called cell extrusion that drives homeostatic epithelial cell death when cells become too crowded. In this work, we show that the pathological crowding of a bronchoconstrictive attack causes so much epithelial cell extrusion that it damages the airways, resulting in inflammation and mucus secretion in both mice and humans. Although relaxing the airways with the rescue treatment albuterol did not affect these responses, inhibiting live cell extrusion signaling during bronchoconstriction prevented all these features. Our findings show that bronchoconstriction causes epithelial damage and inflammation by excess crowding-induced cell extrusion and suggest that blocking epithelial extrusion, instead of the ensuing downstream inflammation, could prevent the feed-forward asthma inflammatory cycle.
    Mesh-Begriff(e) Animals ; Humans ; Mice ; Asthma/pathology ; Asthma/physiopathology ; Bronchoconstriction/drug effects ; Inflammation/pathology ; Signal Transduction ; Ion Channels/antagonists & inhibitors ; Lysophospholipids/antagonists & inhibitors ; Sphingosine/analogs & derivatives ; Sphingosine/antagonists & inhibitors ; Bronchi/pathology ; Bronchi/physiopathology
    Chemische Substanzen Ion Channels ; Piezo1 protein, mouse ; sphingosine 1-phosphate (26993-30-6) ; Lysophospholipids ; Sphingosine (NGZ37HRE42)
    Sprache Englisch
    Erscheinungsdatum 2024-04-04
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.adk2758
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

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  4. Artikel: The RNA binding proteins

    Rynne, Jennifer / Ortiz-Zapater, Elena / Bagley, Dustin C / Zanin, Onofrio / Doherty, George / Kanabar, Varsha / Ward, Jon / Jackson, David J / Parsons, Maddy / Rosenblatt, Jody / Adcock, Ian M / Martinez-Nunez, Rocio T

    Frontiers in cell and developmental biology

    2023  Band 11, Seite(n) 1241008

    Abstract: Introduction: ...

    Abstract Introduction:
    Sprache Englisch
    Erscheinungsdatum 2023-10-19
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1241008
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Bronchoconstriction damages airway epithelia by excess crowding-induced extrusion.

    Bagley, Dustin C / Russell, Tobias / Ortiz-Zapater, Elena / Fox, Kristina / Redd, Paulina Frances / Joseph, Merry / Rice, Cassandra Deering / Reilly, Christopher A / Parsons, Maddy / Rosenblatt, Jody

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Asthma is deemed an inflammatory disease, yet the defining diagnostic symptom is mechanical bronchoconstriction. We previously discovered a conserved process that drives homeostatic epithelial cell death in response to mechanical cell crowding called ... ...

    Abstract Asthma is deemed an inflammatory disease, yet the defining diagnostic symptom is mechanical bronchoconstriction. We previously discovered a conserved process that drives homeostatic epithelial cell death in response to mechanical cell crowding called cell extrusion(1, 2). Here, we show that the pathological crowding of a bronchoconstrictive attack causes so much epithelial cell extrusion that it damages the airways, resulting in inflammation and mucus secretion. While relaxing airways with the rescue treatment albuterol did not impact these responses, inhibiting live cell extrusion signaling during bronchoconstriction prevented all these symptoms. Our findings propose a new etiology for asthma, dependent on the mechanical crowding of a bronchoconstrictive attack. Our studies suggest that blocking epithelial extrusion, instead of ensuing downstream inflammation, could prevent the feed-forward asthma inflammatory cycle.
    Sprache Englisch
    Erscheinungsdatum 2023-08-11
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.08.04.551943
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Epithelial coxsackievirus adenovirus receptor promotes house dust mite-induced lung inflammation.

    Ortiz-Zapater, Elena / Bagley, Dustin C / Hernandez, Virginia Llopis / Roberts, Luke B / Maguire, Thomas J A / Voss, Felizia / Mertins, Philipp / Kirchner, Marieluise / Peset-Martin, Isabel / Woszczek, Grzegorz / Rosenblatt, Jody / Gotthardt, Michael / Santis, George / Parsons, Maddy

    Nature communications

    2022  Band 13, Heft 1, Seite(n) 6407

    Abstract: Airway inflammation and remodelling are important pathophysiologic features in asthma and other respiratory conditions. An intact epithelial cell layer is crucial to maintain lung homoeostasis, and this depends on intercellular adhesion, whilst damaged ... ...

    Abstract Airway inflammation and remodelling are important pathophysiologic features in asthma and other respiratory conditions. An intact epithelial cell layer is crucial to maintain lung homoeostasis, and this depends on intercellular adhesion, whilst damaged respiratory epithelium is the primary instigator of airway inflammation. The Coxsackievirus Adenovirus Receptor (CAR) is highly expressed in the epithelium where it modulates cell-cell adhesion stability and facilitates immune cell transepithelial migration. However, the contribution of CAR to lung inflammation remains unclear. Here we investigate the mechanistic contribution of CAR in mediating responses to the common aeroallergen, House Dust Mite (HDM). We demonstrate that administration of HDM in mice lacking CAR in the respiratory epithelium leads to loss of peri-bronchial inflammatory cell infiltration, fewer goblet-cells and decreased pro-inflammatory cytokine release. In vitro analysis in human lung epithelial cells confirms that loss of CAR leads to reduced HDM-dependent inflammatory cytokine release and neutrophil migration. Epithelial CAR depletion also promoted smooth muscle cell proliferation mediated by GSK3β and TGF-β, basal matrix production and airway hyperresponsiveness. Our data demonstrate that CAR coordinates lung inflammation through a dual function in leucocyte recruitment and tissue remodelling and may represent an important target for future therapeutic development in inflammatory lung diseases.
    Mesh-Begriff(e) Animals ; Humans ; Mice ; Cytokines/metabolism ; Disease Models, Animal ; Inflammation/metabolism ; Lung/metabolism ; Pneumonia/metabolism ; Pyroglyphidae ; Respiratory Mucosa/metabolism ; Receptors, Virus/metabolism
    Chemische Substanzen adenovirus receptor ; Cytokines ; Receptors, Virus
    Sprache Englisch
    Erscheinungsdatum 2022-10-27
    Erscheinungsland England
    Dokumenttyp 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/s41467-022-33882-w
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Mon1a protein acts in trafficking through the secretory apparatus.

    Bagley, Dustin C / Paradkar, Prasad N / Kaplan, Jerry / Ward, Diane M

    The Journal of biological chemistry

    2012  Band 287, Heft 30, Seite(n) 25577–25588

    Abstract: Mon1a was originally identified as a modifier gene of vesicular traffic, as a mutant Mon1a allele resulted in increased localization of cell surface proteins, whereas reduced levels of Mon1a showed decreased secretory activity. Here we show that Mon1a ... ...

    Abstract Mon1a was originally identified as a modifier gene of vesicular traffic, as a mutant Mon1a allele resulted in increased localization of cell surface proteins, whereas reduced levels of Mon1a showed decreased secretory activity. Here we show that Mon1a affects different steps in the secretory pathway including endoplasmic reticulum-to-Golgi traffic. siRNA-dependent reduction of Mon1a levels resulted in a delay in the reformation of the Golgi apparatus after Brefeldin A treatment. Endoglycosidase H treatment of ts045VSVG-GFP confirmed that knockdown of Mon1a delayed endoplasmic reticulum-to-Golgi trafficking. Reductions in Mon1a also resulted in delayed trafficking from Golgi to the plasma membrane. Immunoprecipitation and mass spectrometry analysis showed that Mon1a associates with dynein intermediate chain. Reductions in Mon1a or dynein altered steady state Golgi morphology. Reductions in Mon1a delayed formation of ERGIC-53-positive vesicles, whereas reductions in dynein did not affect vesicle formation. These data provide strong evidence for a role for Mon1a in anterograde trafficking through the secretory apparatus.
    Mesh-Begriff(e) Animals ; Brefeldin A/pharmacology ; COS Cells ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Chlorocebus aethiops ; Dyneins/genetics ; Dyneins/metabolism ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; Glycoside Hydrolases/pharmacology ; Golgi Apparatus/genetics ; Golgi Apparatus/metabolism ; HeLa Cells ; Humans ; Mannose-Binding Lectins/genetics ; Mannose-Binding Lectins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; NIH 3T3 Cells ; Protein Synthesis Inhibitors/pharmacology ; Protein Transport/drug effects ; Protein Transport/physiology ; Secretory Vesicles/genetics ; Secretory Vesicles/metabolism
    Chemische Substanzen Carrier Proteins ; ERGIC-53 protein, mouse ; LMAN1 protein, human ; Mannose-Binding Lectins ; Membrane Proteins ; Mon1a protein, mouse ; Protein Synthesis Inhibitors ; Brefeldin A (20350-15-6) ; Glycoside Hydrolases (EC 3.2.1.-) ; Dyneins (EC 3.6.4.2)
    Sprache Englisch
    Erscheinungsdatum 2012-06-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M112.354043
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Uc I Zs.108: Hefte anzeigen Standort:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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