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dc.creatorWischmann, Johannes
dc.creatorLenze, Florian
dc.creatorThiel, Antonia
dc.creatorBookbinder, Sakina
dc.creatorQuerido, William
dc.creatorSchmidt, Oxana
dc.creatorBurgkart, Rainer
dc.creatorvon Eisenhart-Rothe, Rudiger
dc.creatorRichter, Gunther H. S.
dc.creatorPleshko, Nancy
dc.creatorMayer-Kuckuk, Philipp
dc.date.accessioned2023-06-22T15:11:31Z
dc.date.available2023-06-22T15:11:31Z
dc.date.issued2018-11-01
dc.identifier.issn0014-4827
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/8722
dc.identifier.urihttp://hdl.handle.net/20.500.12613/8758
dc.description.abstractOsteoblasts are adherent cells, and under physiological conditions they attach to both mineralized and non-mineralized osseous surfaces. However, how exactly osteoblasts respond to these different osseous surfaces is largely unknown. Our hypothesis was that the state of matrix mineralization provides a functional signal to osteoblasts. To assess the osteoblast response to mineralized compared to demineralized osseous surfaces, we developed and validated a novel tissue surface model. We demonstrated that with the exception of the absence of mineral, the mineralized and demineralized surfaces were similar in molecular composition as determined, for example, by collagen content and maturity. Subsequently, we used the human osteoblastic cell line MG63 in combination with genome-wide gene set enrichment analysis (GSEA) to record and compare the gene expression signatures on mineralized and demineralized surfaces. Assessment of the 5 most significant gene sets showed on mineralized surfaces an enrichment exclusively of genes sets linked to protein synthesis, while on the demineralized surfaces 3 of the 5 enriched gene sets were associated with the matrix. Focusing on these three gene sets, we observed not only the expected structural components of the bone matrix, but also gene products, such as HMCN1 or NID2, that are likely to act as temporal migration guides. Together, these findings suggest that in osteoblasts mineralized and demineralized osseous surfaces favor intracellular protein production and matrix formation, respectively. Further, they demonstrate that the mineralization state of bone independently controls gene expression in osteoblastic cells.
dc.format.extent10 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartExperimental Cell Research, Vol. 372, Iss. 1
dc.relation.isreferencedbyElsevier
dc.rightsAttribution-NonCommercial-NoDerivs CC BY-NC-ND
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectBone
dc.subjectBone mineral
dc.subjectBone matrix
dc.subjectOsteoblast
dc.subjectGene regulation
dc.titleMatrix mineralization controls gene expression in osteoblastic cells
dc.typeText
dc.type.genreJournal article
dc.description.departmentBioengineering
dc.relation.doihttps://doi.org/10.1016/j.yexcr.2018.09.005
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeTemple University. College of Engineering
dc.creator.orcidQuerido|0000-0002-1484-2415
dc.creator.orcidPleshko|0000-0001-8656-3936
dc.temple.creatorBookbinder, Sakina
dc.temple.creatorQuerido, William
dc.temple.creatorPleshko, Nancy
refterms.dateFOA2023-06-22T15:11:31Z


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