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dc.contributor.author
Franco-Obregón, Alfredo
dc.contributor.author
Wuertz-Kozak, Karin
dc.contributor.author
Spaas, Jan H.
dc.contributor.author
Broeckx, Sarah Y.
dc.contributor.author
Chiers, Koen
dc.contributor.author
Ferguson, Stephen J.
dc.contributor.author
Casarosa, Marco
dc.contributor.author
Bruaene, Nathalie van
dc.contributor.author
Forsyth, Ramses
dc.contributor.author
Duchateau, Luc
dc.date.accessioned
2019-09-30T14:11:20Z
dc.date.available
2017-06-11T19:14:39Z
dc.date.available
2019-09-30T14:11:20Z
dc.date.issued
2015-09
dc.identifier.issn
1015-8987
dc.identifier.issn
1421-9778
dc.identifier.other
10.1159/000430384
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/103983
dc.identifier.doi
10.3929/ethz-b-000103983
dc.description.abstract
Background: Clinical results of regenerative treatments for osteoarthritis are becoming increasingly significant. However, several questions remain unanswered concerning mesenchymal stem cell (MSC) adhesion and incorporation into cartilage. Methods: To this end, peripheral blood (PB) MSCs were chondrogenically induced and/or stimulated with pulsed electromagnetic fields (PEMFs) for a brief period of time just sufficient to prime differentiation. In an organ culture study, PKH26 labelled MSCs were added at two different cell densities (0.5 x106 vs 1.0 x106). In total, 180 explants of six horses (30 per horse) were divided into five groups: no lesion (i), lesion alone (ii), lesion with naïve MSCs (iii), lesion with chondrogenically-induced MSCs (iv) and lesion with chondrogenically-induced and PEMF-stimulated MSCs (v). Half of the explants were mechanically loaded and compared with the unloaded equivalents. Within each circumstance, six explants were histologically evaluated at different time points (day 1, 5 and 14). Results: COMP expression was selectively increased by chondrogenic induction (p = 0.0488). PEMF stimulation (1mT for 10 minutes) further augmented COL II expression over induced values (p = 0.0405). On the other hand, MSC markers remained constant over time after induction, indicating a largely predifferentiated state. In the unloaded group, MSCs adhered to the surface in 92.6% of the explants and penetrated into 40.7% of the lesions. On the other hand, physiological loading significantly reduced surface adherence (1.9%) and lesion filling (3.7%) in all the different conditions (p < 0.0001). Remarkably, homogenous cell distribution was characteristic for chondrogenic induced MSCs (+/- PEMFs), whereas clump formation occurred in 39% of uninduced MSC treated cartilage explants. Finally, unloaded explants seeded with a moderately low density of MSCs exhibited greater lesion filling (p = 0.0022) and surface adherence (p = 0.0161) than explants seeded with higher densities of MSCs. In all cases, the overall amount of lesion filling decreased from day 5 to 14 (p = 0.0156). Conclusion: The present study demonstrates that primed chondrogenic induction of MSCs at a lower cell density without loading results in significantly enhanced and homogenous MSC adhesion and incorporation into equine cartilage.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Karger
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc/3.0/
dc.subject
MSCs
en_US
dc.subject
Cartilage
en_US
dc.subject
Chondrogenic
en_US
dc.subject
Horse
en_US
dc.subject
Peripheral Blood
en_US
dc.title
Chondrogenic Priming at Reduced Cell Density Enhances Cartilage Adhesion of Equine Allogeneic MSCs - a Loading Sensitive Phenomenon in an Organ Culture Study with 180 Explants
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial 3.0 Unported
dc.date.published
2015-09-08
ethz.journal.title
Cellular Physiology and Biochemistry
ethz.journal.volume
37
en_US
ethz.journal.abbreviated
Cell. physiol. biochem.
ethz.pages.start
651
en_US
ethz.pages.end
665
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.nebis
000580750
ethz.publication.place
Basel
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::09597 - Würtz, Karin (SNF-Professur) (ehemalig) / Würtz, Karin (SNF-Professur) (former)
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::03915 - Ferguson, Stephen / Ferguson, Stephen
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::09597 - Würtz, Karin (SNF-Professur) (ehemalig) / Würtz, Karin (SNF-Professur) (former)
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::03915 - Ferguson, Stephen / Ferguson, Stephen
ethz.date.deposited
2017-06-11T19:15:29Z
ethz.source
ECIT
ethz.identifier.importid
imp5936537461ac592474
ethz.ecitpid
pub:162531
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-20T17:19:55Z
ethz.rosetta.lastUpdated
2020-02-15T21:50:04Z
ethz.rosetta.versionExported
true
ethz.COinS
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