Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7968
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dc.contributor.authorMattyasovszky, Stefan-
dc.contributor.authorWollstädter, Jochen-
dc.contributor.authorMartin, Anne-
dc.contributor.authorRitz, Ulrike-
dc.contributor.authorBaranowski, Andreas-
dc.contributor.authorOssendorf, Christian-
dc.contributor.authorRommens, Pol Maria-
dc.contributor.authorHofmann, Alexander-
dc.date.accessioned2022-10-13T07:22:46Z-
dc.date.available2022-10-13T07:22:46Z-
dc.date.issued2016
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7983-
dc.description.abstractBACKGROUND: Contractile myofibroblasts (MFs) accumulate in the joint capsules of patients suffering from posttraumatic joint stiffness. MF activation is controlled by a complex local network of growth factors and cytokines, ending in the increased production of extracellular matrix components followed by soft tissue contracture. Despite the tremendous growth of knowledge in this field, inconsistencies remain in practice and prevention. METHODS AND FINDINGS: In this in vitro study, we isolated and cultured alpha-smooth muscle actin (α-SMA) positive human joint capsule MFs from biopsy specimens and investigated the effect of profibrotic and antifibrotic agents on MF function. Both TGF-β1 and PDGF significantly induced proliferation and increased extracellular matrix contraction in an established 3D collagen gel contraction model. Furthermore, both growth factors induced α-SMA and collagen type I gene expression in MFs. TGF-β1 down-regulated TGF-β1 and TGF-β receptor (R) 1 and receptor (R) 2 gene expression, while PDGF selectively down-regulated TGF-β receptor 2 gene expression. These effects were blocked by suramin. Interestingly, the anti-oxidant agent superoxide dismutase (SOD) blocked TGF-β1 induced proliferation and collagen gel contraction without modulating the gene expression of α-SMA, collagen type I, TGF-β1, TGF-β R1 and TGF-β R2. CONCLUSIONS: Our results provide evidence that targeting the TGF-β1 and PDGF pathways in human joint capsule MFs affects their contractile function. TGF-β1 may modulate MF function in the joint capsule not only via the receptor signalling pathway but also by regulating the production of profibrotic reactive oxygen species (ROS). In particular, anti-oxidant agents could offer promising options in developing strategies for the prevention and treatment of posttraumatic joint stiffness in humans.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleInhibition of contractile function in human joint capsule myofibroblasts by targeting the TGF-β1 and PDGF pathwaysen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7968-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLoS onede
jgu.journal.volume11de
jgu.journal.issue1de
jgu.pages.alternativee0145948de
jgu.publisher.year2016-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0145948de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-03-02T08:17:20Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Klinik und Poliklinik für Unfallchirurgiede_DE
opus.organisation.stringFB 04: Medizin: Orthopädische Klinik und Poliklinikde_DE
opus.identifier.opusid56244
opus.institute.number0439
opus.institute.number0443
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedMattyasovszky, Stefan
opus.affiliatedRitz, Ulrike
opus.affiliatedBaranowski, Andreas
opus.affiliatedRommens, Pol Maria
opus.affiliatedHofmann, Alexander
jgu.publisher.doi10.1371/journal.pone.0145948de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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