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dc.contributor.authorCarvalho, Marta S.
dc.contributor.authorSilva, João C.
dc.contributor.authorHoff, Christopher M.
dc.contributor.authorCabral, Joaquim M.S.
dc.contributor.authorLinhardt, Robert J.
dc.contributor.authorda Silva, Cláudia L.
dc.contributor.authorVashishth, Deepak
dc.date2020
dc.date.accessioned2022-06-27T15:40:48Z
dc.date.available2022-06-27T15:40:48Z
dc.date.issued2020-10-01
dc.identifier.citationLoss and rescue of osteocalcin and osteopontin modulate osteogenic and angiogenic features of mesenchymal stem/stromal cells, M. S. Carvalho, J. C. Silva, C. Hoff, J.M. S. Cabral, R. J. Linhardt, C. Lobato da Silva, D. Vashishth, Journal of Cellular Physiology, 235, 7496–7515, 2020.
dc.identifier.issn10974652
dc.identifier.issn219541
dc.identifier.urihttps://doi.org/10.1002/jcp.29653
dc.identifier.urihttps://hdl.handle.net/20.500.13015/5488
dc.descriptionJournal of Cellular Physiology, 235, 7496–7515
dc.descriptionNote : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
dc.description.abstractNoncollagenous proteins in the bone extracellular matrix, such as osteocalcin (OC) and osteopontin (OPN), inherent to evolution of bone as a skeletal tissue, are known to regulate bone formation and mineralization. However, the fundamental basis of this regulatory role remains unknown. Here, for the first time, we use mouse mesenchymal stem/stromal cells (MSC) lacking both OC and OPN to investigate the mechanistic roles of OC and OPN on the proliferation capacity and differentiation ability of MSC. We found that the loss of OC and OPN reduces stem cells self-renewal potential and multipotency, affects their differentiation into an osteogenic lineage, and impairs their angiogenic potential while maintaining chondrogenic and adipogenic lineages. Moreover, loss of OC and OPN compromises the extracellular matrix integrity and maturation, observed by an unexpected enhancement of glycosaminoglycans content that are associated with a more primitive skeletal connective tissue, and by a delay on the maturation of mineral species produced. Interestingly, exogenously supplemented OC and OPN were able to rescue MSC proliferative and osteogenic potential along with matrix integrity and mineral quality. Taken together, these results highlight the key contributions of OC and OPN in enhancing osteogenesis and angiogenesis over primitive connective tissue, and support a potential therapeutic approach based on their exogenous supplementation.
dc.description.sponsorshipNational Institutes of Health
dc.description.urihttps://login.libproxy.rpi.edu/login?url=https://doi.org/10.1002/jcp.29653
dc.languageen_US
dc.language.isoENG
dc.relation.ispartofThe Linhardt Research Labs Online Collection
dc.relation.ispartofRensselaer Polytechnic Institute, Troy, NY
dc.relation.ispartofJournal of Cellular Physiology
dc.relation.urihttps://harc.rpi.edu/
dc.subjectBiology
dc.subjectChemistry and chemical biology
dc.subjectChemical and biological engineering
dc.subjectBiomedical engineering
dc.titleLoss and rescue of osteocalcin and osteopontin modulate osteogenic and angiogenic features of mesenchymal stem/stromal cells
dc.typeArticle
dcterms.accessRightshttps://login.libproxy.rpi.edu/login?url=https://doi.org/10.1002/jcp.29653
dcterms.isPartOfJournal
dcterms.isVersionOfhttps://doi.org/10.1002/jcp.29653
dc.rights.holderIn Copyright : this Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). https://rightsstatements.org/page/InC/1.0/
dc.creator.identifierhttps://orcid.org/0000-0003-2219-5833
dc.relation.departmentThe Linhardt Research Labs.
dc.relation.departmentThe Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
rpi.description.pages7496-7515
rpi.description.volume235


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