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      Zinc-modified Calcium Silicate Coatings Promote Osteogenic Differentiation through TGF-β/Smad Pathway and Osseointegration in Osteopenic Rabbits

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          Abstract

          Surface-modified metal implants incorporating different ions have been employed in the biomedical field as bioactive dental implants with good osseointegration properties. However, the molecular mechanism through which surface coatings exert the biological activity is not fully understood, and the effects have been difficult to achieve, especially in the osteopenic bone. In this study, We examined the effect of zinc-modified calcium silicate coatings with two different Zn contents to induce osteogenic differentiation of rat bone marrow-derived pericytes (BM-PCs) and osteogenetic efficiency in ovariectomised rabbits. Ti-6Al-4V with zinc-modified calcium silicate coatings not only enhanced proliferation but also promoted osteogenic differentiation and mineralized matrix deposition of rat BM-PCs as the zinc content and culture time increased in vitro. The associated molecular mechanisms were investigated by Q-PCR and Western blotting, revealing that TGF-β/Smad signaling pathway plays a direct and significant role in regulating BM-PCs osteoblastic differentiation on Zn-modified coatings. Furthermore, in vivo results that revealed Zn-modified calcium silicate coatings significantly promoted new bone formation around the implant surface in osteopenic rabbits as the Zn content and exposure time increased. Therefore, Zn-modified calcium silicate coatings can improve implant osseointegration in the condition of osteopenia, which may be beneficial for patients suffering from osteoporosis-related fractures.

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          Most cited references 71

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          Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation.

          The osteoblast is the bone-forming cell. The molecular basis of osteoblast-specific gene expression and differentiation is unknown. We previously identified an osteoblast-specific cis-acting element, termed OSE2, in the Osteocalcin promoter. We have now cloned the cDNA encoding Osf2/Cbfa1, the protein that binds to OSE2. Osf2/Cbfa1 expression is initiated in the mesenchymal condensations of the developing skeleton, is strictly restricted to cells of the osteoblast lineage thereafter, and is regulated by BMP7 and vitamin D3. Osf2/Cbfa1 binds to and regulates the expression of multiple genes expressed in osteoblasts. Finally, forced expression of Osf2/Cbfa1 in nonosteoblastic cells induces the expression of the principal osteoblast-specific genes. This study identifies Osf2/Cbfa1 as an osteoblast-specific transcription factor and as a regulator of osteoblast differentiation.
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            TGF-beta signalling from cell membrane to nucleus through SMAD proteins.

            The recent identification of the SMAD family of signal transducer proteins has unravelled the mechanisms by which transforming growth factor-beta (TGF-beta) signals from the cell membrane to the nucleus. Pathway-restricted SMADs are phosphorylated by specific cell-surface receptors that have serine/threonine kinase activity, then they oligomerize with the common mediator Smad4 and translocate to the nucleus where they direct transcription to effect the cell's response to TGF-beta. Inhibitory SMADs have been identified that block the activation of these pathway-restricted SMADs.
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              Cbfa1, a candidate gene for cleidocranial dysplasia syndrome, is essential for osteoblast differentiation and bone development.

              We have generated Cbfa1-deficient mice. Homozygous mutants die of respiratory failure shortly after birth. Analysis of their skeletons revealed an absence of osteoblasts and bone. Heterozygous mice showed specific skeletal abnormalities that are characteristic of the human heritable skeletal disorder, cleidocranial dysplasia (CCD). These defects are also observed in a mouse Ccd mutant for this disease. The Cbfa1 gene was shown to be deleted in the Ccd mutation. Analysis of embryonic Cbfa1 expression using a lacZ reporter gene revealed strong expression at sites of bone formation prior to the earliest stages of ossification. Thus, the Cbfa1 gene is essential for osteoblast differentiation and bone formation, and the Cbfa1 heterozygous mouse is a paradigm for a human skeletal disorder.
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                Author and article information

                Contributors
                yjm_st@163.com
                061022049@fudan.edu.cn
                yespine@163.com
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                13 June 2017
                13 June 2017
                2017
                : 7
                Affiliations
                [1 ]ISNI 0000 0004 0369 1660, GRID grid.73113.37, Department of Orthopaedics, , Changzheng Hospital of Second Military Medical University, ; Shanghai, 200003 China
                [2 ]ISNI 0000000119573309, GRID grid.9227.e, Key Laboratory of Inorganic Coating Materials, Shanghai Institute of Ceramics, , Chinese Academy of Sciences, ; Shanghai, 200050 China
                [3 ]ISNI 0000 0004 0369 6365, GRID grid.22069.3f, Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, , East China Normal University, ; Shanghai, 200241 China
                [4 ]National Engineering Research Center for Nanotechnology, Shanghai, 200241 China
                Article
                3661
                10.1038/s41598-017-03661-5
                5469779
                28611362
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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