TGF-beta-induced SOCS3 expression augments TNF-alpha-induced osteoclast formation
dc.contributor.author | Lovibond, AC | |
dc.contributor.author | Haque, SJ | |
dc.contributor.author | Chambers, TJ | |
dc.contributor.author | Fox, Simon | |
dc.date.accessioned | 2023-02-15T15:37:48Z | |
dc.date.available | 2023-02-15T15:37:48Z | |
dc.date.issued | 2003-01-01 | |
dc.identifier.issn | 0006-291X | |
dc.identifier.issn | 1090-2104 | |
dc.identifier.uri | http://hdl.handle.net/10026.1/20393 | |
dc.description.abstract |
Osteoclast differentiation is dependent on TGF-beta to prime precursors to the osteoclast lineage. The mechanism by which TGF-beta enables osteoclast formation is unknown. One possibility is that TGF-beta opposes pro-inflammatory JAK/STAT signalling. Recently, we showed that TGF-beta-induces SOCS3, an inhibitor of the JAK/STAT pathway, in precursors and enhances SOCS3 in RANKL-induced osteoclasts. We therefore elected to test the role of SOCS3 in the effect of other regulators of osteoclastic differentiation. We found that TNF-alpha-induced osteoclasts also express SOCS3 and TGF-beta strongly up-regulates this. Moreover, TNF-alpha-induced osteoclast differentiation and total resorbed bone area were enhanced in SOCS3-retrovirally infected precursors, whereas antisense knockdown of SOCS3 suppressed formation and the augmentative effect of TGF-beta. Furthermore, SOCS3 overexpression blunted the anti-osteoclastic effect of IFN-beta but not IL-10. This suggests that TGF-beta-induced expression of SOCS3 may represent a crucial mechanism by which TGF-beta antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions. | |
dc.format.extent | 762-767 | |
dc.format.medium | ||
dc.language | en | |
dc.language.iso | en | |
dc.publisher | Elsevier BV | |
dc.subject | osteoclast | |
dc.subject | lineage-commitment | |
dc.subject | TGF-beta | |
dc.subject | SOCS3 | |
dc.subject | TNF-alpha | |
dc.title | TGF-beta-induced SOCS3 expression augments TNF-alpha-induced osteoclast formation | |
dc.type | journal-article | |
dc.type | Article | |
plymouth.author-url | https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000185774300008&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008 | |
plymouth.issue | 4 | |
plymouth.volume | 309 | |
plymouth.publication-status | Published | |
plymouth.journal | Biochemical and Biophysical Research Communications | |
dc.identifier.doi | 10.1016/j.bbrc.2003.08.068 | |
plymouth.organisational-group | /Plymouth | |
plymouth.organisational-group | /Plymouth/Faculty of Health | |
plymouth.organisational-group | /Plymouth/Faculty of Health/School of Biomedical Sciences | |
plymouth.organisational-group | /Plymouth/Research Groups | |
plymouth.organisational-group | /Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED) | |
plymouth.organisational-group | /Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR | |
plymouth.organisational-group | /Plymouth/Research Groups/Plymouth Institute of Health and Care Research (PIHR) | |
plymouth.organisational-group | /Plymouth/Users by role | |
plymouth.organisational-group | /Plymouth/Users by role/Academics | |
dc.publisher.place | United States | |
dc.identifier.eissn | 1090-2104 | |
dc.rights.embargoperiod | Not known | |
rioxxterms.versionofrecord | 10.1016/j.bbrc.2003.08.068 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.type | Journal Article/Review |