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dc.contributor.author
Martino, Mikaël M.
dc.contributor.author
Maruyama, Kenta
dc.contributor.author
Kuhn, Gisela A.
dc.contributor.author
Satoh, Takashi
dc.contributor.author
Takeuchi, Osamu
dc.contributor.author
Müller, Ralph
dc.contributor.author
Akira, Shizuo
dc.date.accessioned
2018-09-12T08:00:52Z
dc.date.available
2017-06-12T02:33:08Z
dc.date.available
2018-09-12T08:00:52Z
dc.date.issued
2016
dc.identifier.other
10.1038/ncomms11051
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/114095
dc.identifier.doi
10.3929/ethz-b-000114095
dc.description.abstract
Tissue injury and the healing response lead to the release of endogenous danger signals including Toll-like receptor (TLR) and interleukin-1 receptor, type 1 (IL-1R1) ligands, which modulate the immune microenvironment. Because TLRs and IL-1R1 have been shown to influence the repair process of various tissues, we explored their role during bone regeneration, seeking to design regenerative strategies integrating a control of their signalling. Here we show that IL-1R1/MyD88 signalling negatively regulates bone regeneration, in the mouse. Furthermore, IL-1β which is released at the bone injury site, inhibits the regenerative capacities of mesenchymal stem cells (MSCs). Mechanistically, IL-1R1/MyD88 signalling impairs MSC proliferation, migration and differentiation by inhibiting the Akt/GSK-3β/β-catenin pathway. Lastly, as a proof of concept, we engineer a MSC delivery system integrating inhibitors of IL-1R1/MyD88 signalling. Using this strategy, we considerably improve MSC-based bone regeneration in the mouse, demonstrating that this approach may be useful in regenerative medicine applications.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Nature Publishing Group
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.title
Inhibition of IL-1R1/MyD88 signalling promotes mesenchymal stem cell-driven tissue regeneration
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2016-03-22
ethz.journal.title
Nature Communications
ethz.journal.volume
7
en_US
ethz.pages.start
11051
en_US
ethz.size
13 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.identifier.nebis
007044158
ethz.publication.place
London
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::03565 - Müller, Ralph / Müller, Ralph
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::03565 - Müller, Ralph / Müller, Ralph
ethz.date.deposited
2017-06-12T02:35:32Z
ethz.source
ECIT
ethz.identifier.importid
imp59365436ecc6a53249
ethz.ecitpid
pub:175867
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-31T15:43:10Z
ethz.rosetta.lastUpdated
2019-02-03T07:52:46Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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