Transforming growth factor-β enables NFATc1 expression during osteoclastogenesis
dc.contributor.author | Fox, Simon | |
dc.contributor.author | Evans, KE | |
dc.contributor.author | Lovibond, AC | |
dc.date.accessioned | 2023-02-15T15:31:15Z | |
dc.date.available | 2023-02-15T15:31:15Z | |
dc.date.issued | 2008-02 | |
dc.identifier.issn | 0006-291X | |
dc.identifier.issn | 1090-2104 | |
dc.identifier.uri | http://hdl.handle.net/10026.1/20390 | |
dc.description.abstract |
Osteoclastogenesis is dependent on distinct stimuli that prime and activate osteoclast differentiation. One cytokine needed to prime monocytes for osteoclastogenesis is TGF-beta, which enables and augments RANKL and TNF-alpha-induced osteoclast differentiation. However, the precise time-period during which this occurs and the molecular mechanism mediating this action are unknown. We report here TGF-beta prime monocytes for osteoclast formation within 24h by regulating expression of NFATc1, a key osteoclastic transcription factor. TGF-beta directly induces cytoplasmic NFATc1 expression within 24h, but is unable to stimulate NFATc1 nuclear translocation. Furthermore, RANKL-induced NFATc1 expression is dependent on the presence of TGF-beta during the early stages of osteoclastogenesis. Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1. In light of these findings, it is apparent that osteoclast formation is dependent on coordinated interactions between TGF-beta and RANKL/TNF-alpha that regulate the expression and intracellular distribution of NFATc1 during early stages of osteoclast differentiation. | |
dc.format.extent | 123-128 | |
dc.format.medium | Print-Electronic | |
dc.language | en | |
dc.language.iso | eng | |
dc.publisher | Elsevier BV | |
dc.subject | osteoclast | |
dc.subject | TGF-beta | |
dc.subject | priming | |
dc.subject | NFATc1 | |
dc.subject | monocyte differentiation | |
dc.title | Transforming growth factor-β enables NFATc1 expression during osteoclastogenesis | |
dc.type | journal-article | |
dc.type | Journal Article | |
dc.type | Research Support, Non-U.S. Gov't | |
plymouth.author-url | https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000252392400020&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008 | |
plymouth.issue | 1 | |
plymouth.volume | 366 | |
plymouth.publication-status | Published | |
plymouth.journal | Biochemical and Biophysical Research Communications | |
dc.identifier.doi | 10.1016/j.bbrc.2007.11.120 | |
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 | |
dcterms.dateAccepted | 2007-11-19 | |
dc.identifier.eissn | 1090-2104 | |
dc.rights.embargoperiod | Not known | |
rioxxterms.versionofrecord | 10.1016/j.bbrc.2007.11.120 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.licenseref.startdate | 2008-02-01 | |
rioxxterms.type | Journal Article/Review |