High glucose alters the secretome of mechanically stimulated osteocyte-like cells affecting osteoclast precursor recruitment and differentiation

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dc.contributor.authorMaycas, Marta
dc.contributor.authorPortolés Pérez, María Teresa
dc.contributor.authorMatesanz Sancho, María Concepción
dc.contributor.authorBuendía, Irene
dc.contributor.authorLinares, Javier
dc.contributor.authorFeito Castellano, María José
dc.contributor.authorArcos Navarrete, Daniel
dc.contributor.authorVallet Regí, María Dulce Nombre
dc.contributor.authorPlotkin, Lilian I.
dc.contributor.authorEsbrit, Pedro
dc.contributor.authorGortázar, Arancha R.
dc.date.accessioned2023-06-17T22:07:01Z
dc.date.available2023-06-17T22:07:01Z
dc.date.issued2017-12
dc.description.abstractDiabetes mellitus (DM) induces bone deterioration, while mechanical stimulation promotes osteocyte-driven bone formation. We aimed to evaluate the interaction of acute exposure (24 h) to high glucose (HG) with both the pro-survival effect conferred to osteocytic MLO-Y4 cells and osteoblastic MC3T3-E1 cells by mechanical stimulation and the interaction of these cells with osteoclast precursor RAW264.7 cells. We found that 24 h of HG (25 mM) preexposure prevented both cell survival and ERK and β-catenin nuclear translocation upon mechanical stimulation by fluid flow (FF) (10 min) in both MLO-Y4 and MC3T3-E1 cells. However, migration of RAW 264.7 cells was inhibited by MLO-Y4 cell-conditioned medium (CM), but not by MC3T3-E1 cell-CM, with HG or FF. This inhibitory effect was associated with consistent changes in VEGF, RANTES, MIP-1α, MIP-1β MCP-1, and GM-CSF in MLO-Y4 cellCM. RAW264.7 proliferation was inhibited by MLO-Y4 CM under static or HG conditions, but it increased by FF-CM with or without HG. In addition, both FF and HG abrogated the capacity of RAW 264.7 cells to differentiate into osteoclasts, but in a different manner. Thus, HG-CM in static condition allowed formation of osteoclast-like cells, which were unable to resorb hydroxyapatite. In contrast, FF-CM prevented osteoclastogenesis even in HG condition. Moreover, HG did not affect basal RANKL or IL-6 secretion or their inhibition induced by FF in MLO-Y4 cells. In conclusion, this in vitro study demonstrates that HG exerts disparate effects on osteocyte mechanotransduction, and provides a novel mechanism by which DM disturbs skeletal metabolism through altered osteocyte-osteoclast communication.
dc.description.departmentSección Deptal. de Bioquímica y Biología Molecular (Biológicas)
dc.description.facultyFac. de Ciencias Biológicas
dc.description.refereedTRUE
dc.description.sponsorshipUnión Europea. H2020
dc.description.sponsorshipMinisterio de Ciencia e Innovación (MICINN)
dc.description.sponsorshipMinisterio de Economía y Competitividad (MINECO)
dc.description.sponsorshipUniversidad San Pablo CEU (Emerging Group)
dc.description.statuspub
dc.eprint.idhttps://eprints.ucm.es/id/eprint/44713
dc.identifier.doi10.1002/jcp.25829
dc.identifier.issn0021-9541, ESSN: 1097-4652
dc.identifier.officialurlhttp://onlinelibrary.wiley.com/doi/10.1002/jcp.25829/full
dc.identifier.urihttps://hdl.handle.net/20.500.14352/18086
dc.issue.number12
dc.journal.titleJournal of Cellular Physiology
dc.language.isoeng
dc.page.final3621
dc.page.initial3611
dc.publisherWiley
dc.relation.projectIDVERDI (694160)
dc.relation.projectIDMAT2012-35556
dc.relation.projectID(MAT2013-43299-R, MAT2015-64831-R and MAT2016-75611-R )
dc.relation.projectID(FI12/00458)
dc.rights.accessRightsopen access
dc.subject.cdu577.1
dc.subject.cdu612.75
dc.subject.keywordDiabetes mellitus
dc.subject.keywordMechanotransduction
dc.subject.keywordOsteoclast migration
dc.subject.keywordOsteoclastogenesis
dc.subject.keywordOsteocyte
dc.subject.ucmFisiología
dc.subject.ucmBioquímica (Biología)
dc.subject.unesco2411 Fisiología Humana
dc.subject.unesco2302 Bioquímica
dc.titleHigh glucose alters the secretome of mechanically stimulated osteocyte-like cells affecting osteoclast precursor recruitment and differentiation
dc.typejournal article
dc.volume.number232
dspace.entity.typePublication
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relation.isAuthorOfPublication216318f7-e25a-4850-b122-856eb08b3e2f
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relation.isAuthorOfPublication.latestForDiscovery4b317058-0bd1-4fd8-afab-5fa79a4b7002
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