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  1. Book ; Thesis: Effect of TGF-β1 on barrier function of lung epithelia

    Schilpp, Carolin

    2021  

    Title variant TGF-beta-1 ; Effect of TGF-beta 1 on barrier function of lung epithelia
    Institution Universität Ulm
    Author's details submitted by Carolin Schilpp
    Keywords $DE-289 ; Respiratory tract infections ; Respiratory mucosa ; Transforming growth factors
    Language English
    Size XIII, 99 Blätter, Illustrationen, Diagramme (teilweise farbig)
    Publishing place Ulm
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Universität Ulm, 2021
    HBZ-ID HT021129855
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2021 E 1328 order for loan Magazin
    2023 E 226 order for loan Magazin

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  2. Article ; Online: TGF-β1 increases permeability of ciliated airway epithelia via redistribution of claudin 3 from tight junction into cell nuclei.

    Schilpp, Carolin / Lochbaum, Robin / Braubach, Peter / Jonigk, Danny / Frick, Manfred / Dietl, Paul / Wittekindt, Oliver H

    Pflugers Archiv : European journal of physiology

    2021  Volume 473, Issue 2, Page(s) 287–311

    Abstract: TGF-β1 is a major mediator of airway tissue remodelling during atopic asthma and affects tight junctions (TJs) of airway epithelia. However, its impact on TJs of ciliated epithelia is sparsely investigated. Herein we elaborated effects of TGF-β1 on TJs ... ...

    Abstract TGF-β1 is a major mediator of airway tissue remodelling during atopic asthma and affects tight junctions (TJs) of airway epithelia. However, its impact on TJs of ciliated epithelia is sparsely investigated. Herein we elaborated effects of TGF-β1 on TJs of primary human bronchial epithelial cells. We demonstrate that TGF-β1 activates TGF-β1 receptors TGFBR1 and TGFBR2 resulting in ALK5-mediated phosphorylation of SMAD2. We observed that TGFBR1 and -R2 localize specifically on motile cilia. TGF-β1 activated accumulation of phosphorylated SMAD2 (pSMAD2-C) at centrioles of motile cilia and at cell nuclei. This triggered an increase in paracellular permeability via cellular redistribution of claudin 3 (CLDN3) from TJs into cell nuclei followed by disruption of epithelial integrity and formation of epithelial lesions. Only ciliated cells express TGF-β1 receptors; however, nuclear accumulations of pSMAD2-C and CLDN3 redistribution were observed with similar time course in ciliated and non-ciliated cells. In summary, we demonstrate a role of motile cilia in TGF-β1 sensing and showed that TGF-β1 disturbs TJ permeability of conductive airway epithelia by redistributing CLDN3 from TJs into cell nuclei. We conclude that the observed effects contribute to loss of epithelial integrity during atopic asthma.
    MeSH term(s) Bronchi/drug effects ; Bronchi/metabolism ; Cells, Cultured ; Cilia/drug effects ; Cilia/metabolism ; Claudin-3/genetics ; Claudin-3/metabolism ; Electric Impedance ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Permeability ; Phosphorylation ; Protein Transport ; Receptor, Transforming Growth Factor-beta Type I/agonists ; Receptor, Transforming Growth Factor-beta Type I/metabolism ; Receptor, Transforming Growth Factor-beta Type II/agonists ; Receptor, Transforming Growth Factor-beta Type II/metabolism ; Signal Transduction ; Smad2 Protein/metabolism ; Tight Junctions/drug effects ; Tight Junctions/genetics ; Tight Junctions/metabolism ; Transforming Growth Factor beta1/pharmacology
    Chemical Substances CLDN3 protein, human ; Claudin-3 ; SMAD2 protein, human ; Smad2 Protein ; Transforming Growth Factor beta1 ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Receptor, Transforming Growth Factor-beta Type II (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30) ; TGFBR2 protein, human (EC 2.7.11.30)
    Language English
    Publishing date 2021-01-02
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-020-02501-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Pharmacological cholesterol depletion disturbs ciliogenesis and ciliary function in developing zebrafish.

    Maerz, Lars D / Burkhalter, Martin D / Schilpp, Carolin / Wittekindt, Oliver H / Frick, Manfred / Philipp, Melanie

    Communications biology

    2019  Volume 2, Page(s) 31

    Abstract: Patients with an inherited inability to synthesize sufficient amounts of cholesterol develop congenital malformations of the skull, toes, kidney and heart. As development of these structures depends on functional cilia we investigated whether cholesterol ...

    Abstract Patients with an inherited inability to synthesize sufficient amounts of cholesterol develop congenital malformations of the skull, toes, kidney and heart. As development of these structures depends on functional cilia we investigated whether cholesterol regulates ciliogenesis through inhibition of hydroxymethylglutaryl-Coenzyme A reductase (HMG-CoA-R), the rate-limiting enzyme in cholesterol synthesis. HMG-CoA-R is efficiently inhibited by statins, a standard medication for hyperlipidemia. When zebrafish embryos are treated with statins cilia dysfunction phenotypes including heart defects, left-right asymmetry defects and malformation of ciliated organs develop, which are ameliorated by cholesterol replenishment. HMG-CoA-R inhibition and other means of cholesterol reduction lowered ciliation frequency and cilia length in zebrafish as well as several mammalian cell types. Cholesterol depletion further triggers an inability for ciliary signalling. Because of a reduction of the transition zone component Pi(4,5)P
    MeSH term(s) Animals ; Atorvastatin/pharmacology ; Cholesterol/metabolism ; Cilia/drug effects ; Cilia/metabolism ; Ciliopathies/etiology ; Ciliopathies/metabolism ; Humans ; Organogenesis/genetics ; Phenotype ; Zebrafish/embryology ; Zebrafish/metabolism
    Chemical Substances Cholesterol (97C5T2UQ7J) ; Atorvastatin (A0JWA85V8F)
    Language English
    Publishing date 2019-01-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-018-0272-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Retinoic acid signalling adjusts tight junction permeability in response to air-liquid interface conditions.

    Lochbaum, Robin / Schilpp, Carolin / Nonnenmacher, Lara / Frick, Manfred / Dietl, Paul / Wittekindt, Oliver H

    Cellular signalling

    2019  Volume 65, Page(s) 109421

    Abstract: The pulmonary epithelium separates the gaseous intraluminal space of the airways and the aqueous interstitium. This compartimentalization is required for appropriate lung function, it is established during perinatal periods and can be disturbed in lung ... ...

    Abstract The pulmonary epithelium separates the gaseous intraluminal space of the airways and the aqueous interstitium. This compartimentalization is required for appropriate lung function, it is established during perinatal periods and can be disturbed in lung edema. Herein we elaborated the impact of the air-liquid interface (ALI) on the function of the pulmonary epithelium. We used NCI-H441 epithelia as a well-established and characterized model of distal airway epithelia, which were cultivated either at ALI or (at submerged conditions) at liquid-liquid interface conditions (LLI). Our study revealed that paracellular permeability was increased and claudin 1 (CLDN1) expression levels were reduced under LLI conditions. This was accompanied by elevated c-FOS, c-JUN and retinoic acid receptor α (RARA) expression, as well as cellular retinoic acid (RA) content. Exposure of epithelia to RA derivatives of ALI cultivated epithelia mimicked effects of LLI. The increase in RA content was in line with the identified upregulation of retinoic acid anabolizing enzymes ALDH1A3 and DHRS3. CLDN1 promoter analysis revealed c-FOS and c-JUN as activating transcription factors, whereas activation of RARA reduced CLDN1 promoter activity. We then concluded that ALI/LLI dependent modulation of CLDN1 expression and TJ permeability is under the control of RA synthesis. Activation of RARA results in an inhibition of c-FOS/c-JUN dependent CLDN1 promoter activation and increased TJ permeability. Our results underscore RA signalling as a pivotal mechanism in adjusting TJ properties, which could play a role during birth when the lung changes from LLI to ALI conditions.
    MeSH term(s) Aldehyde Oxidoreductases/metabolism ; Claudin-1/genetics ; Claudin-1/metabolism ; HEK293 Cells ; Humans ; Lung/drug effects ; Lung/metabolism ; Lung/physiology ; Permeability/drug effects ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/physiology ; Retinoic Acid Receptor alpha/genetics ; Retinoic Acid Receptor alpha/metabolism ; Signal Transduction ; Tight Junctions/drug effects ; Tight Junctions/metabolism ; Tight Junctions/physiology ; Transcriptional Activation/drug effects ; Tretinoin/metabolism ; Tretinoin/pharmacology ; Up-Regulation
    Chemical Substances CLDN1 protein, human ; Claudin-1 ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; RARA protein, human ; Retinoic Acid Receptor alpha ; Tretinoin (5688UTC01R) ; Aldehyde Oxidoreductases (EC 1.2.-) ; aldehyde dehydrogenase (NAD(P)+) (EC 1.2.1.5)
    Language English
    Publishing date 2019-09-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2019.109421
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2579: 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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  5. Article ; Online: IL-13 Impairs Tight Junctions in Airway Epithelia.

    Schmidt, Hanna / Braubach, Peter / Schilpp, Carolin / Lochbaum, Robin / Neuland, Kathrin / Thompson, Kristin / Jonigk, Danny / Frick, Manfred / Dietl, Paul / Wittekindt, Oliver H

    International journal of molecular sciences

    2019  Volume 20, Issue 13

    Abstract: Interleukin-13 (IL-13) drives symptoms in asthma with high levels of T-helper type 2 cells ( ... ...

    Abstract Interleukin-13 (IL-13) drives symptoms in asthma with high levels of T-helper type 2 cells (T
    MeSH term(s) Cells, Cultured ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Interleukin-13/pharmacology ; Janus Kinases/metabolism ; Proteasome Endopeptidase Complex/metabolism ; STAT Transcription Factors/metabolism ; Tight Junctions/drug effects ; Tight Junctions/metabolism ; Trachea/cytology ; Trachea/metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitination
    Chemical Substances Interleukin-13 ; STAT Transcription Factors ; UBE2Z protein, human (EC 2.3.2.23) ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23) ; Janus Kinases (EC 2.7.10.2) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2019-06-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20133222
    Database MEDical Literature Analysis and Retrieval System OnLINE

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