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dc.contributor.author
Wunderli, Stefania
dc.contributor.author
Blache, Ulrich
dc.contributor.author
Beretta Piccoli, Agnese
dc.contributor.author
Niederöst, Barbara
dc.contributor.author
Holenstein, Claude N.
dc.contributor.author
Passini, Fabian S.
dc.contributor.author
Silvan, Unai
dc.contributor.author
Bundgaard, Louise
dc.contributor.author
auf dem Keller, Ulrich
dc.contributor.author
Snedeker, Jess Gerrit
dc.date.accessioned
2020-06-10T09:19:49Z
dc.date.available
2020-01-31T09:19:22Z
dc.date.available
2020-01-31T11:20:59Z
dc.date.available
2020-06-10T09:19:49Z
dc.date.issued
2020-07
dc.identifier.issn
0945-053X
dc.identifier.issn
1569-1802
dc.identifier.other
10.1016/j.matbio.2019.12.003
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/396082
dc.identifier.doi
10.3929/ethz-b-000396082
dc.description.abstract
Although the molecular mechanisms behind tendon disease remain obscure, aberrant stromal matrix turnover and tissue hypervascularity are known hallmarks of advanced tendinopathy. We harness a tendon explant model to unwind complex cross-talk between the stromal and vascular tissue compartments. We identify the hypervascular tendon niche as a state-switch that gates degenerative matrix remodeling within the tissue stroma. Here pathological conditions resembling hypervascular tendon disease provoke rapid cell-mediated tissue breakdown upon mechanical unloading, in contrast to unloaded tendons that remain functionally stable in physiological low-oxygen/-temperature niches. Analyses of the stromal tissue transcriptome and secretome reveal that a stromal niche with elevated tissue oxygenation and temperature drives a ROS mediated cellular stress response that leads to adoption of an immune-modulatory phenotype within the degrading stromal tissue. Degradomic analysis further reveals a surprisingly rich set of active matrix proteases behind the progressive loss of tissue mechanics. We conclude that the tendon stromal compartment responds to aberrant mechanical unloading in a manner that is highly dependent on the vascular niche, with ROS gating a complex proteolytic breakdown of the functional collagen backbone.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Elsevier
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject
Tendon
en_US
dc.subject
Explant
en_US
dc.subject
Reactive oxygen species (ROS)
en_US
dc.subject
Proteases
en_US
dc.subject
Tissue model
en_US
dc.title
Tendon response to matrix unloading is determined by the patho-physiological niche
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
dc.date.published
2020-01-07
ethz.journal.title
Matrix Biology
ethz.journal.volume
89
en_US
ethz.pages.start
11
en_US
ethz.pages.end
26
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Oxford
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02070 - Dep. Gesundheitswiss. und Technologie / Dep. of Health Sciences and Technology::02518 - Institut für Biomechanik / Institute for Biomechanics::03822 - Snedeker, Jess G. / Snedeker, Jess G.
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02070 - Dep. Gesundheitswiss. und Technologie / Dep. of Health Sciences and Technology::02518 - Institut für Biomechanik / Institute for Biomechanics::03822 - Snedeker, Jess G. / Snedeker, Jess G.
en_US
ethz.date.deposited
2020-01-31T09:19:30Z
ethz.source
FORM
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-06-10T09:19:59Z
ethz.rosetta.lastUpdated
2021-02-15T14:30:03Z
ethz.rosetta.versionExported
true
ethz.COinS
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