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  1. Article: A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.

    Keeler, Shamus P / Wu, Kangyun / Zhang, Yong / Mao, Dailing / Li, Ming / Iberg, Courtney A / Austin, Stephen R / Glaser, Samuel A / Yantis, Jennifer / Podgorny, Stephanie / Brody, Steven L / Chartock, Joshua R / Han, Zhenfu / Byers, Derek E / Romero, Arthur G / Holtzman, Michael J

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Common respiratory diseases continue to represent a major public health problem, and much of the morbidity and mortality is due to airway inflammation and mucus production. Previous studies indicated a role for mitogen-activated protein kinase 14 (MAPK14) ...

    Abstract Common respiratory diseases continue to represent a major public health problem, and much of the morbidity and mortality is due to airway inflammation and mucus production. Previous studies indicated a role for mitogen-activated protein kinase 14 (MAPK14) in this type of disease, but clinical trials are unsuccessful to date. Our previous work identified a related but distinct kinase known as MAPK13 that is activated in respiratory airway diseases and is required for mucus production in human cell-culture models. Support for MAPK13 function in these models came from effectiveness of
    Language English
    Publishing date 2023-10-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.26.542451
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.

    Keeler, Shamus P / Wu, Kangyun / Zhang, Yong / Mao, Dailing / Li, Ming / Iberg, Courtney A / Austin, Stephen R / Glaser, Samuel A / Yantis, Jennifer / Podgorny, Stephanie / Brody, Steven L / Chartock, Joshua R / Han, Zhenfu / Byers, Derek E / Romero, Arthur G / Holtzman, Michael J

    American journal of physiology. Lung cellular and molecular physiology

    2023  Volume 325, Issue 6, Page(s) L726–L740

    Abstract: Common respiratory diseases continue to represent a major public health problem, and much of the morbidity and mortality is due to airway inflammation and mucus production. Previous studies indicated a role for mitogen-activated protein kinase 14 (MAPK14) ...

    Abstract Common respiratory diseases continue to represent a major public health problem, and much of the morbidity and mortality is due to airway inflammation and mucus production. Previous studies indicated a role for mitogen-activated protein kinase 14 (MAPK14) in this type of disease, but clinical trials are unsuccessful to date. Our previous work identified a related but distinct kinase known as MAPK13 that is activated in respiratory airway diseases and is required for mucus production in human cell-culture models. Support for MAPK13 function in these models came from effectiveness of
    MeSH term(s) Animals ; Humans ; Swine ; Mitogen-Activated Protein Kinase 14/metabolism ; Swine, Miniature/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; Inflammation/drug therapy ; Inflammation/metabolism ; Mucus/metabolism ; Cytokines/metabolism ; Mitogen-Activated Protein Kinase 13/metabolism
    Chemical Substances Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24) ; Cytokines ; Mitogen-Activated Protein Kinase 13 (EC 2.7.1.-)
    Language English
    Publishing date 2023-10-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00183.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Chloride channel accessory 1 gene deficiency causes selective loss of mucus production in a new pig model.

    Keeler, Shamus P / Yantis, Jennifer / Gerovac, Benjamin J / Youkilis, Samuel L / Podgorny, Stephanie / Mao, Dailing / Zhang, Yong / Whitworth, Kristin M / Redel, Bethany / Samuel, Melissa S / Wells, Kevin D / Prather, Randall S / Holtzman, Michael J

    American journal of physiology. Lung cellular and molecular physiology

    2022  Volume 322, Issue 6, Page(s) L842–L852

    Abstract: Morbidity and mortality of respiratory diseases are linked to airway obstruction by mucus but there are still no specific, safe, and effective drugs to correct this phenotype. The need for better treatment requires a new understanding of the basis for ... ...

    Abstract Morbidity and mortality of respiratory diseases are linked to airway obstruction by mucus but there are still no specific, safe, and effective drugs to correct this phenotype. The need for better treatment requires a new understanding of the basis for mucus production. In that regard, studies of human airway epithelial cells in primary culture show that a mucin granule constituent known as chloride channel accessory 1 (CLCA1) is required for inducible expression of the inflammatory mucin MUC5AC in response to potent type 2 cytokines. However, it remained uncertain whether CLCLA1 is necessary for mucus production in vivo. Conventional approaches to functional biology using targeted gene knockout were difficult due to the functional redundancy of additional
    MeSH term(s) Animals ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Epithelial Cells/metabolism ; Goblet Cells/metabolism ; Lung/metabolism ; Mice ; Mucin 5AC/genetics ; Mucin 5AC/metabolism ; Mucus/metabolism ; Respiratory Mucosa/metabolism ; Swine
    Chemical Substances Chloride Channels ; Mucin 5AC
    Language English
    Publishing date 2022-04-19
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00443.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.A 2749: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Basal epithelial stem cells cross an alarmin checkpoint for postviral lung disease.

    Wu, Kangyun / Kamimoto, Kenji / Zhang, Yong / Yang, Kuangying / Keeler, Shamus P / Gerovac, Benjamin J / Agapov, Eugene V / Austin, Stephen P / Yantis, Jennifer / Gissy, Kelly A / Byers, Derek E / Alexander-Brett, Jennifer / Hoffmann, Christy M / Wallace, Matthew / Hughes, Michael E / Crouch, Erika C / Morris, Samantha A / Holtzman, Michael J

    The Journal of clinical investigation

    2021  Volume 131, Issue 19

    Abstract: Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here, we recognized a pattern of imbalance marked by basal epithelial cell growth ... ...

    Abstract Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here, we recognized a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaced normal airspaces in a mouse model of progressive postviral lung disease due to the Sendai virus. Single-cell and lineage-tracing technologies identified a distinct subset of basal epithelial stem cells (basal ESCs) that extended into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset was selectively expanded by crossing a cell-growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that was independent of IL-33 receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il33 gene function in basal epithelial cells disrupted the homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuated postviral disease in the lung based on the downregulation of remodeling and inflammation. Thus, we define a basal ESC strategy to deploy innate immune machinery that appears to overshoot the primordial goal of self-defense. Our findings reveal new targets to stratify and correct chronic and often deadly postviral disease.
    MeSH term(s) Alarmins/physiology ; Animals ; Cell Differentiation ; Epithelial Cells/physiology ; Interleukin-33/genetics ; Interleukin-33/physiology ; Lung Diseases/physiopathology ; Mice ; Respirovirus Infections/complications ; Sendai virus ; Single-Cell Analysis ; Stem Cells/cytology ; Stem Cells/physiology
    Chemical Substances Alarmins ; Interleukin-33
    Language English
    Publishing date 2021-07-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI149336
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.184: Show issues Location:
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