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  1. Article ; Online: Sfrp1 inhibits lung fibroblast invasion during transition to injury-induced myofibroblasts.

    Mayr, Christoph H / Sengupta, Arunima / Asgharpour, Sara / Ansari, Meshal / Pestoni, Jeanine C / Ogar, Paulina / Angelidis, Ilias / Liontos, Andreas / Rodriguez-Castillo, José Alberto / Lang, Niklas J / Strunz, Maximilian / Porras-Gonzalez, Diana / Gerckens, Michael / De Sadeleer, Laurens J / Oehrle, Bettina / Viteri-Alvarez, Valeria / Fernandez, Isis E / Tallquist, Michelle / Irmler, Martin /
    Beckers, Johannes / Eickelberg, Oliver / Stoleriu, Gabriel Mircea / Behr, Jürgen / Kneidinger, Nikolaus / Wuyts, Wim A / Wasnick, Roxana Maria / Yildirim, Ali Önder / Ahlbrecht, Katrin / Morty, Rory E / Samakovlis, Christos / Theis, Fabian J / Burgstaller, Gerald / Schiller, Herbert B

    The European respiratory journal

    2024  Volume 63, Issue 2

    Abstract: Background: Fibroblast-to-myofibroblast conversion is a major driver of tissue remodelling in organ fibrosis. Distinct lineages of fibroblasts support homeostatic tissue niche functions, yet their specific activation states and phenotypic trajectories ... ...

    Abstract Background: Fibroblast-to-myofibroblast conversion is a major driver of tissue remodelling in organ fibrosis. Distinct lineages of fibroblasts support homeostatic tissue niche functions, yet their specific activation states and phenotypic trajectories during injury and repair have remained unclear.
    Methods: We combined spatial transcriptomics, multiplexed immunostainings, longitudinal single-cell RNA-sequencing and genetic lineage tracing to study fibroblast fates during mouse lung regeneration. Our findings were validated in idiopathic pulmonary fibrosis patient tissues
    Measurements and main results: We discovered a transitional fibroblast state characterised by high
    Conclusions: Our study reveals the convergence of spatially and transcriptionally distinct fibroblast lineages into transcriptionally uniform myofibroblasts and identifies SFRP1 as a modulator of TGFβ1-driven fibroblast phenotypes in fibrogenesis. These findings are relevant in the context of therapeutic interventions that aim at limiting or reversing fibroblast foci formation.
    MeSH term(s) Mice ; Animals ; Humans ; Myofibroblasts/metabolism ; Fibroblasts/metabolism ; Lung/metabolism ; Idiopathic Pulmonary Fibrosis/metabolism ; Cell Differentiation ; Transforming Growth Factor beta1/metabolism ; Extracellular Matrix Proteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism
    Chemical Substances Transforming Growth Factor beta1 ; CTHRC1 protein, human ; Extracellular Matrix Proteins ; Sfrp1 protein, mouse ; Membrane Proteins
    Language English
    Publishing date 2024-02-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01326-2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2322: 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)
    Zs.MO 292: Show issues

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  2. Article ; Online: CX3CR1-fractalkine axis drives kinetic changes of monocytes in fibrotic interstitial lung diseases.

    Greiffo, Flavia R / Viteri-Alvarez, Valeria / Frankenberger, Marion / Dietel, Daniela / Ortega-Gomez, Almudena / Lee, Joyce S / Hilgendorff, Anne / Behr, Jürgen / Soehnlein, Oliver / Eickelberg, Oliver / Fernandez, Isis E

    The European respiratory journal

    2020  Volume 55, Issue 2

    Abstract: Circulating immune cell populations have been shown to contribute to interstitial lung disease (ILD). In this study, we analysed circulating and lung resident monocyte populations, and assessed their phenotype and recruitment from the blood to the lung ... ...

    Abstract Circulating immune cell populations have been shown to contribute to interstitial lung disease (ILD). In this study, we analysed circulating and lung resident monocyte populations, and assessed their phenotype and recruitment from the blood to the lung in ILD. Flow cytometry analysis of blood samples for quantifying circulating monocytes was performed in 105 subjects: 83 with ILD (n=36, n=28 and n=19 for nonspecific interstitial pneumonia, hypersensitivity pneumonitis and connective-tissue disease-associated ILD, respectively), as well as 22 controls. Monocyte localisation and abundance were assessed using immunofluorescence and flow cytometry of lung tissue. Monocyte populations were cultured either alone or with endothelial cells to assess fractalkine-dependent transmigration pattern. We show that circulating classical monocytes (CM) were increased in ILD compared with controls, while nonclassical monocytes (NCM) were decreased. CM abundance correlated inversely with lung function, while NCM abundance correlated positively. Both CCL2 and CX3CL1 concentrations were increased in plasma and lungs of ILD patients. Fractalkine co-localised with ciliated bronchial epithelial cells, thereby creating a chemoattractant gradient towards the lung. Fractalkine enhanced endothelial transmigration of NCM in ILD samples only. Immunofluorescence, as well as flow cytometry, showed an increased presence of NCM in fibrotic niches in ILD lungs. Moreover, NCM in the ILD lungs expressed increased CX3CR1, M2-like and phagocytic markers. Taken together, our data support that in ILD, fractalkine drives the migration of CX3CR1
    MeSH term(s) CX3C Chemokine Receptor 1 ; Chemokine CX3CL1 ; Endothelial Cells ; Flow Cytometry ; Humans ; Lung Diseases, Interstitial ; Monocytes
    Chemical Substances CX3C Chemokine Receptor 1 ; CX3CR1 protein, human ; Chemokine CX3CL1
    Language English
    Publishing date 2020-02-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.00460-2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2322: 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)
    Zs.MO 292: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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