Relevant bibliographies by topics / Osteoblast

Academic literature on the topic 'Osteoblast'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "Osteoblast"

1

Kim, Jung Ha, Kabsun Kim, Inyoung Kim, Semun Seong, Jeong-Tae Koh, and Nacksung Kim. "The ATF3–OPG Axis Contributes to Bone Formation by Regulating the Differentiation of Osteoclasts, Osteoblasts, and Adipocytes." International Journal of Molecular Sciences 23, no. 7 (March 23, 2022): 3500. http://dx.doi.org/10.3390/ijms23073500.

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Activating transcription factor 3 (ATF3) has been identified as a negative regulator of osteoblast differentiation in in vitro study. However, it was not associated with osteoblast differentiation in in vivo study. To provide an understanding of the discrepancy between the in vivo and in vitro findings regarding the function of ATF3 in osteoblasts, we investigated the unidentified roles of ATF3 in osteoblast biology. ATF3 enhanced osteoprotegerin (OPG) production, not only in osteoblast precursor cells, but also during osteoblast differentiation and osteoblastic adipocyte differentiation. In addition, ATF3 increased nodule formation in immature osteoblasts and decreased osteoblast-dependent osteoclast formation, as well as the transdifferentiation of osteoblasts to adipocytes. However, all these effects were reversed by the OPG neutralizing antibody. Taken together, these results suggest that ATF3 contributes to bone homeostasis by regulating the differentiation of various cell types in the bone microenvironment, including osteoblasts, osteoclasts, and adipocytes via inducing OPG production.
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2

Giuliani, Nicola, Francesca Morandi, Sara Tagliaferri, Mirca Lazzaretti, Sabrina Bonomini, Monica Crugnola, Cristina Mancini, et al. "The proteasome inhibitor bortezomib affects osteoblast differentiation in vitro and in vivo in multiple myeloma patients." Blood 110, no. 1 (July 1, 2007): 334–38. http://dx.doi.org/10.1182/blood-2006-11-059188.

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The proteasome inhibitor bortezomib may increase osteoblast-related markers in multiple myeloma (MM) patients; however, its potential osteoblastic stimulatory effect is not known. In this study, we show that bortezomib significantly induced a stimulatory effect on osteoblast markers in human mesenchymal cells without affecting the number of osteoblast progenitors in bone marrow cultures or the viability of mature osteoblasts. Consistently we found that bortezomib significantly increased the transcription factor Runx2/Cbfa1 activity in human osteoblast progenitors and osteoblasts without affecting nuclear and cytoplasmatic active β-catenin levels. Consequently a stimulatory effect of bortezomib on bone nodule formation was also demonstrated in osteoblast progenitors. These in vitro observations were confirmed in vivo by the finding of a significant increase in the number of osteoblastic cells × mm2 of bone tissue and in the number of Runx2/Cbfa1-positive osteoblastic cells that was observed in MM patients who responded to bortezomib. Our in vitro and in vivo observations support the hypothesis that a direct stimulatory effect on bone formation process could occur during bortezomib treatment.
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Bauer, Omri, Amnon Sharir, Ayako Kimura, Shay Hantisteanu, Shu Takeda, and Yoram Groner. "Loss of Osteoblast Runx3 Produces Severe Congenital Osteopenia." Molecular and Cellular Biology 35, no. 7 (January 20, 2015): 1097–109. http://dx.doi.org/10.1128/mcb.01106-14.

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Congenital osteopenia is a bone demineralization condition that is associated with elevated fracture risk in human infants. Here we show thatRunx3, likeRunx2, is expressed in precommitted embryonic osteoblasts and that Runx3-deficient mice develop severe congenital osteopenia. Runx3-deficient osteoblast-specific (Runx3fl/fl/Col1α1-cre), but not chondrocyte-specific (Runx3fl/fl/Col1α2-cre), mice are osteopenic. This demonstrates that an osteoblastic cell-autonomous function of Runx3 is required for proper osteogenesis. Bone histomorphometry revealed that decreased osteoblast numbers and reduced mineral deposition capacity in Runx3-deficient mice cause this bone formation deficiency. Neonatal bone and cultured primary osteoblast analyses revealed a Runx3-deficiency-associated decrease in the number of active osteoblasts resulting from diminished proliferation and not from enhanced osteoblast apoptosis. These findings are supported by Runx3-null culture transcriptome analyses showing significant decreases in the levels of osteoblastic markers and increases in the levels of Notch signaling components. Thus, while Runx2 is mandatory for the osteoblastic lineage commitment, Runx3 is nonredundantly required for the proliferation of these precommitted cells, to generate adequate numbers of active osteoblasts. HumanRUNX3resides on chromosome 1p36, a region that is associated with osteoporosis. Therefore, RUNX3 might also be involved in human bone mineralization.
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Ducy, P., and G. Karsenty. "Two distinct osteoblast-specific cis-acting elements control expression of a mouse osteocalcin gene." Molecular and Cellular Biology 15, no. 4 (April 1995): 1858–69. http://dx.doi.org/10.1128/mcb.15.4.1858.

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Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regulatory elements required for osteoblast-specific expression. Three different binding sites, called A, B, and C, for factors present in nuclear extracts of osteoblasts were identified in this short promoter by DNase I footprint assays. In gel retardation assays, the A element, located between bp -64 and -47, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing primary osteoblasts. The B element, located between bp -110 and -83, bound a ubiquitously expressed factor. The C element, located between bp -146 and -132, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing and mineralizing primary osteoblasts. When cloned upstream of a minimum osteocalcin promoter or a heterologous promoter, multimers of the A element strongly increased the activities of these promoters in osteoblastic cell lines at two different stages of differentiation but in no other cell line; we named this element osteocalcin-specific element 1 (OSE1). Multimers of the C element increased the activities of these promoters predominantly in a differentiated osteoblastic cell line; we named this element OSE2. This study demonstrates that two distinct cis-acting elements are responsible for osteoblast expression of mOG2 and provides for the first time a functional characterization of osteoblast-specific cis-acting elements. We speculate that these two elements may be important at several stages of osteoblast differentiation.
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Sutton, Amelia L. M., Xiaoxue Zhang, Diane R. Dowd, Yogendra P. Kharode, Barry S. Komm, and Paul N. MacDonald. "Semaphorin 3B Is a 1,25-Dihydroxyvitamin D3-Induced Gene in Osteoblasts that Promotes Osteoclastogenesis and Induces Osteopenia in Mice." Molecular Endocrinology 22, no. 6 (June 1, 2008): 1370–81. http://dx.doi.org/10.1210/me.2007-0363.

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Abstract The vitamin D endocrine system is important for skeletal homeostasis. 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] impacts bone indirectly by promoting intestinal absorption of calcium and phosphate and directly by acting on osteoblasts and osteoclasts. Despite the direct actions of 1,25(OH)2D3 in bone, relatively little is known of the mechanisms or target genes that are regulated by 1,25(OH)2D3 in skeletal cells. Here, we identify semaphorin 3B (SEMA3B) as a 1,25(OH)2D3-stimulated gene in osteoblastic cells. Northern analysis revealed strong induction of SEMA3B mRNA by 1,25(OH)2D3 in MG-63, ST-2, MC3T3, and primary osteoblastic cells. Moreover, differentiation of these osteogenic cells enhanced SEMA3B gene expression. Biological effects of SEMA3B in the skeletal system have not been reported. Here, we show that osteoblast-derived SEMA3B alters global skeletal homeostasis in intact animals and osteoblast function in cell culture. Osteoblast-targeted expression of SEMA3B in mice resulted in reduced bone mineral density and aberrant trabecular structure compared with nontransgenic littermates. Histomorphometry studies indicated that this was likely due to increased osteoclast numbers and activity. Indeed, primary osteoblasts obtained from SEMA3B transgenic mice stimulated osteoclastogenesis to a greater extent than nontransgenic osteoblasts. This study establishes that SEMA3B is a 1,25(OH)2D3-induced gene in osteoblasts and that osteoblast-derived SEMA3B impacts skeletal biology in vitro and in vivo. Collectively, these studies support a putative role for SEMA3B as an osteoblast protein that regulates bone mass and skeletal homeostasis.
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Skillington, Jeremy, Lisa Choy, and Rik Derynck. "Bone morphogenetic protein and retinoic acid signaling cooperate to induce osteoblast differentiation of preadipocytes." Journal of Cell Biology 159, no. 1 (October 14, 2002): 135–46. http://dx.doi.org/10.1083/jcb.200204060.

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Mesenchymal cells can differentiate into osteoblasts, adipocytes, myoblasts, or chondroblasts. Whether mesenchymal cells that have initiated differentiation along one lineage can transdifferentiate into another is largely unknown. Using 3T3-F442A preadipocytes, we explored whether extracellular signals could redirect their differentiation from adipocyte into osteoblast. 3T3-F442A cells expressed receptors and Smads required for bone morphogenetic protein (BMP) signaling. BMP-2 increased proliferation and induced the early osteoblast differentiation marker alkaline phosphatase, yet only mildly affected adipogenic differentiation. Retinoic acid inhibited adipose conversion and cooperated with BMP-2 to enhance proliferation, inhibit adipogenesis, and promote early osteoblastic differentiation. Expression of BMP-RII together with BMP-RIA or BMP-RIB suppressed adipogenesis of 3T3-F442A cells and promoted full osteoblastic differentiation in response to retinoic acid. Osteoblastic differentiation was characterized by induction of cbfa1, osteocalcin, and collagen I expression, and extracellular matrix calcification. These results indicate that 3T3-F442A preadipocytes can be converted into fully differentiated osteoblasts in response to extracellular signaling cues. Furthermore, BMP and retinoic acid signaling cooperate to stimulate cell proliferation, repress adipogenesis, and promote osteoblast differentiation. Finally, BMP-RIA and BMP-RIB induced osteoblast differentiation and repressed adipocytic differentiation to a similar extent.
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Hernández-Tapia, Laura G., Zdenka Fohlerová, Jan Žídek, Marco A. Alvarez-Perez, Ladislav Čelko, Jozef Kaiser, and Edgar B. Montufar. "Effects of Cryopreservation on Cell Metabolic Activity and Function of Biofabricated Structures Laden with Osteoblasts." Materials 13, no. 8 (April 22, 2020): 1966. http://dx.doi.org/10.3390/ma13081966.

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Biofabrication and maturation of bone constructs is a long-term task that requires a high degree of specialization. This specialization falls onto the hierarchy complexity of the bone tissue that limits the transfer of this technology to the clinic. This work studied the effects of the short-term cryopreservation on biofabricated osteoblast-containing structures, with the final aim to make them steadily available in biobanks. The biological responses studied include the osteoblast post-thawing metabolic activity and the recovery of the osteoblastic function of 3D-bioprinted osteoblastic structures and beta tricalcium phosphate (β-TCP) scaffolds infiltrated with osteoblasts encapsulated in a hydrogel. The obtained structures were cryopreserved at −80 °C for 7 days using dimethyl sulfoxide (DMSO) as cryoprotectant additive. After thawing the structures were cultured up to 14 days. The results revealed fundamental biological aspects for the successful cryopreservation of osteoblast constructs. In summary, immature osteoblasts take longer to recover than mature osteoblasts. The pre-cryopreservation culture period had an important effect on the metabolic activity and function maintain, faster recovering normal values when cryopreserved after longer-term culture (7 days). The use of β-TCP scaffolds further improved the osteoblast survival after cryopreservation, resulting in similar levels of alkaline phosphatase activity in comparison with the non-preserved structures. These results contribute to the understanding of the biology of cryopreserved osteoblast constructs, approaching biofabrication to the clinical practice.
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Kim, Jung Ha, Kabsun Kim, Inyoung Kim, Semun Seong, Hyun Kook, Kyung Keun Kim, Jeong-Tae Koh, and Nacksung Kim. "Bifunctional Role of CrkL during Bone Remodeling." International Journal of Molecular Sciences 22, no. 13 (June 29, 2021): 7007. http://dx.doi.org/10.3390/ijms22137007.

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Coupled signaling between bone-forming osteoblasts and bone-resorbing osteoclasts is crucial to the maintenance of bone homeostasis. We previously reported that v-crk avian sarcoma virus CT10 oncogene homolog-like (CrkL), which belongs to the Crk family of adaptors, inhibits bone morphogenetic protein 2 (BMP2)-mediated osteoblast differentiation, while enhancing receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation. In this study, we investigated whether CrkL can also regulate the coupling signals between osteoblasts and osteoclasts, facilitating bone homeostasis. Osteoblastic CrkL strongly decreased RANKL expression through its inhibition of runt-related transcription factor 2 (Runx2) transcription. Reduction in RANKL expression by CrkL in osteoblasts resulted in the inhibition of not only osteoblast-dependent osteoclast differentiation but also osteoclast-dependent osteoblast differentiation, suggesting that CrkL participates in the coupling signals between osteoblasts and osteoclasts via its regulation of RANKL expression. Therefore, CrkL bifunctionally regulates osteoclast differentiation through both a direct and indirect mechanism while it inhibits osteoblast differentiation through its blockade of both BMP2 and RANKL reverse signaling pathways. Collectively, these data suggest that CrkL is involved in bone homeostasis, where it helps to regulate the complex interactions of the osteoblasts, osteoclasts, and their coupling signals.
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Yu, Vionnie W. C., Gourgen Ambartsoumian, Lieve Verlinden, Janet M. Moir, Josée Prud'homme, Claude Gauthier, Peter J. Roughley, and René St-Arnaud. "FIAT represses ATF4-mediated transcription to regulate bone mass in transgenic mice." Journal of Cell Biology 169, no. 4 (May 23, 2005): 591–601. http://dx.doi.org/10.1083/jcb.200412139.

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We report the characterization of factor inhibiting activating transcription factor 4 (ATF4)–mediated transcription (FIAT), a leucine zipper nuclear protein. FIAT interacted with ATF4 to inhibit binding of ATF4 to DNA and block ATF4-mediated transcription of the osteocalcin gene in vitro. Transgenic mice overexpressing FIAT in osteoblasts also had reduced osteocalcin gene expression and decreased bone mineral density, bone volume, mineralized volume, trabecular thickness, trabecular number, and decreased rigidity of long bones. Mineral homeostasis, osteoclast number and activity, and osteoblast proliferation and apoptosis were unchanged in transgenics. Expression of osteoblastic differentiation markers was largely unaffected and type I collagen synthesis was unchanged. Mineral apposition rate was reduced in transgenic mice, suggesting that the lowered bone mass was due to a decline in osteoblast activity. This cell-autonomous decrease in osteoblast activity was confirmed by measuring reduced alkaline phosphatase activity and mineralization in primary osteoblast cultures. These results show that FIAT regulates bone mass accrual and establish FIAT as a novel transcriptional regulator of osteoblastic function.
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Giuliani, Nicola, Francesca Morandi, Sara Tagliaferri, Mirca Lazzaretti, Sabrina Bonomini, Monica Crugnola, Daniela Petrò, Cristina Mancini, Eugenia Martella, and Vittorio Rizzoli. "The Proteasome Inhibitor Bortezomib Affects Osteoblastogenesis and Bone Formation In Vitro and In Vivo in Multiple Myeloma Patients." Blood 108, no. 11 (November 16, 2006): 508. http://dx.doi.org/10.1182/blood.v108.11.508.508.

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Abstract It is well established that osteoblast formation and function are profoundly impaired in multiple myeloma (MM) patients. Osteoblastic cells also regulate myeloma cell growth and increasing bone formation result in a reduction of tumoral burden in mice. Recent data suggest that ubiquitin-proteasome pathway, the major cellular degradative system and therapeutic target in myeloma cells, also regulates osteoblast differentiation. Further it has been demonstrated that different proteasome inhibitors may stimulate bone formation in mice. Finally, preliminary observations obtained in MM patients treated with the proteasome inhibitor Bortezomib show an increase of bone specific alkaline phosphatase in responder patients as compared to non-responder ones. Currently it is not know whether the proteasome inhibitor Bortezomib may have a direct effect on osteoblast and bone formation in vitro human cultures and in vivo in MM patients. To clarify this issue first we checked the effect of Bortezomib either on osteoblast differentiation and formation or on osteoblast proliferation, survival and function. In long-term human BM cultures we found that Bortezomib did not reduce the number of both early bone marrow (BM) osteoblast progenitors Colony Forming Unit-Fibroblast (CFU-F) and late ones Colony Forming Bone nodules (CFU-OB). On the other hand we found that Bortezomib (2–3 nM) significantly induced osteoblast phenotype in human mesenchymal cells incubated in presence of osteogenic factors. A stimulatory effect on osteoblast markers was observed after 24 hours of Bortezomib treatment. Consistently we found that Bortezomib significantly increased the activity of the transcription factor Runx2/Cbfa1 in human osteoblast progenitors without affecting the canonical WNT signaling pathway checked by the evaluation of nuclear and cytoplasmatic active beta-catenin levels. Using the human osteoblast like cells MG-63 and immortalized normal osteoblasts (HOBIT) we found that Bortezomib at concentration ranging between 2nM and 5nM did not inhibit osteoblast proliferation or induce osteoblast apoptosis. Similarly, Bortezomib did not affect the expression of osteoblast markers, Runx2/Cbfa1 activity and WNT signaling in both MG-63 and HOBIT cells. To extent our in vitro observation we have evaluated the potential effect of Bortezomib in vivo in MM patients. Bone histomorphometry as well as immunostainig for Runx2/Cbfa1 and beta-catenin was performed on BM biopsies obtained from 15 MM patients before and after 6–8 cycles of Bortezomib administrated in mono-therapy. A significant increase in the number of osteoblastic cells X mm2 of bone tissue and in the number of Runx2/Cbfa1 positive osteoblastic cells was observed only in responder patients showing an early increase of the serum alkaline phosphatase. In conclusion our data indicate that Bortezomib may increase osteoblast differentiation in human mesenchymal cells without affecting the proliferation, survival and function of mature osteoblasts. In vivo and in vitro observations support the hypothesis that both direct and indirect effects on bone formation process could occur during Bortezomib treatment.
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Dissertations / Theses on the topic "Osteoblast"

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McManus, Lindsay L. "A study of human mesenchymal stem cells, human primary osteoblasts and osteoblast-like cells using Raman spectroscopy." Thesis, University of Ulster, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.551188.

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Raman spectroscopy is a vibrational spectroscopy technique that provides a global biochemical signature and has been shown to have utility in the analysis of biological cells for bone tissue engineering applications. Traditionally, sample analysis in this field employs destructive biological methods that require the use of biomarkers, however, Raman has since become an essential tool in various areas of bio-industry and by incorporating the technique into biological laboratories these perturbing methodologies are no longer the only means of analysis. Therefore the focus of this study was to investigate the capability of Raman spectroscopy as a tool for the in vitro characterisation of the sub-cellular composition and osteogenic potential of human mesenchymal stem cells. As with most biological samples a high degree of heterogeneity is often found, therefore in order to extract the desired information from the biological studies multivariate analysis tools were utilised. The reliability and consistency of the vibrational analysis was confirmed by means of comparison with current gold-standard techniques such as, alizarin red staining, real-time polymerase chain reaction and immunocytochemistry. A further novelty was introduced with the use of Raman spectroscopy to determine the suitability of the U20S osteoblast-like cell line for use as a model for human primary osteoblasts with emphasis on the ability of these cell types to replicate their tissue of origin. Investigation of the U20S osteoblast-like cell line provided evidence of dense multilayered mineralised regions that corresponded more closely to native bone, which has not been previously reported on. This finding contradicts previous reports on U20S osteoblast-like cells which have consistently been described as non-osteoinductive. When Raman spectroscopy is coupled with biological and multivariate analyses techniques, it shows further novelty when employed to monitor mineralisation of human mesenchymal stem cells, human primary osteoblasts and osteoblast-like cells. This body of work culminates the success of a truly multidisciplinary approach and provides the potential for further work on bone cell analysis and the applications of spectroscopy for biological studies and bone tissue engineering applications.
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Hempel, Ute, Carolin Preissler, Sarah Vogel, Stephanie Möller, Vera Hintze, Jana Becher, Matthias Schnabelrauch, Martina Rauner, Lorenz C. Hofbauer, and Peter Dieter. "Artificial Extracellular Matrices with Oversulfated Glycosaminoglycan Derivatives Promote the Differentiation of Osteoblast-Precursor Cells and Premature Osteoblasts." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-165309.

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Sulfated glycosaminoglycans (GAG) are components of the bone marrow stem cell niche and to a minor extent of mature bone tissue with important functions in regulating stem cell lineage commitment and differentiation. We anticipated that artificial extracellular matrices (aECM) composed of collagen I and synthetically oversulfated GAG derivatives affect preferentially the differentiation of osteoblast-precursor cells and early osteoblasts. A set of gradually sulfated chondroitin sulfate and hyaluronan derivatives was used for the preparation of aECM. All these matrices were analysed with human bone marrow stromal cells to identify the most potent aECM and to determine the influence of the degree and position of sulfate groups and the kind of disaccharide units on the osteogenic differentiation. Oversulfated GAG derivatives with a sulfate group at the C-6 position of the N-acetylglycosamine revealed the most pronounced proosteogenic effect as determined by tissue nonspecific alkaline phosphatase activity and calcium deposition. A subset of the aECM was further analysed with different primary osteoblasts and cell lines reflecting different maturation stages to test whether the effect of sulfated GAG derivatives depends on the maturation status of the cells. It was shown that the proosteogenic effect of aECMwasmost prominent in early osteoblasts. [ABSTRACT FROM AUTHOR]
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Hempel, Ute, Carolin Preissler, Sarah Vogel, Stephanie Möller, Vera Hintze, Jana Becher, Matthias Schnabelrauch, Martina Rauner, Lorenz C. Hofbauer, and Peter Dieter. "Artificial Extracellular Matrices with Oversulfated Glycosaminoglycan Derivatives Promote the Differentiation of Osteoblast-Precursor Cells and Premature Osteoblasts." Hindawi, 2014. https://tud.qucosa.de/id/qucosa%3A28669.

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Sulfated glycosaminoglycans (GAG) are components of the bone marrow stem cell niche and to a minor extent of mature bone tissue with important functions in regulating stem cell lineage commitment and differentiation. We anticipated that artificial extracellular matrices (aECM) composed of collagen I and synthetically oversulfated GAG derivatives affect preferentially the differentiation of osteoblast-precursor cells and early osteoblasts. A set of gradually sulfated chondroitin sulfate and hyaluronan derivatives was used for the preparation of aECM. All these matrices were analysed with human bone marrow stromal cells to identify the most potent aECM and to determine the influence of the degree and position of sulfate groups and the kind of disaccharide units on the osteogenic differentiation. Oversulfated GAG derivatives with a sulfate group at the C-6 position of the N-acetylglycosamine revealed the most pronounced proosteogenic effect as determined by tissue nonspecific alkaline phosphatase activity and calcium deposition. A subset of the aECM was further analysed with different primary osteoblasts and cell lines reflecting different maturation stages to test whether the effect of sulfated GAG derivatives depends on the maturation status of the cells. It was shown that the proosteogenic effect of aECMwasmost prominent in early osteoblasts. [ABSTRACT FROM AUTHOR]
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Duque, Gustavo. "Molecular changes in the aging osteoblast." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19466.

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Aging is the consequence ofan array of phenotypic variations that appear to involve intrinsic or constitutional properties in all cells and systems, including qualitative and quantitative alterations in development, maturational structure and function. The aging process in bone involves a set ofchanges in bone cells differentiation, interaction and premature death. Osteoblasts are the cells most affected during the aging process in bone due to their complex mechanisms ofdifferentiation, their interaction with honnones and growth factors and their progression to apoptosis.
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Townsend, Paul Andrew. "The molecular basis of osteoblast adhesion." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263651.

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Boonphayak, Piyanan. "Substituted hydroxyapatite analysis of osteoblast response." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/substituted-hydroxyapatite-analysis-of-osteoblast-response(71ddb64d-03b9-4825-875e-61d68bd2d3e6).html.

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Ceramics used for medical purposes are known as bioceramics, such as hydroxyaptite (HA), which is one of the most well studied bioceramics because of its similar composition to human bone and also good biocompatibility, is bioactive and has excellent osteoconductivity. In addition many properties of HA can be improved by the addition of specific elements into its structure. The research in this thesis investigates the substitution of some selected elements into the structure of HA and subsequent characterisation in terms of physical, mechanical and biological responses. Si/S-HA and Sr/B/S-HA was obtained from Lucideon and Ho/HA was synthesised in house. Initially a cell response to a variety of element oxides was performed to identify elements to avoid or potentially use for substitution. Dysprosium (Dy), erbium (Er), europium (Eu), gadolinium (Gd), holmium (Ho) and praseodymium (Pr) at 100 ppm showed better results for alkaline phosphatase activity than 25 ppm in culture medium.2.5 and 5 mol.% of Ho was substituted into HA structure using a wet chemical method of synthesis. The samples were sintered at 1200°C for 10 hours. There was high crystallinity when 2.5 mol.% of Ho was added into the HA structure. Substitution of Ho in HA structure had the effect of shortening in a axis and elongation in c axis along with the higher concentration of Ho ion.2 mol.% of Si and S was also substituted into HA structure, where both elements Si and S replace PO4 site in HA structure. Si substituted in SiO4 form and S substituted in SO4 form for PO4 as confirmed by FT-IR results. Osteoblast-like cells cultured on Si/S-HA showed an increase in alkaline phosphatase, collagen type I and ostecalcin on samples sintered at high temperature. Sr/B/S-HA was also made where 2 mol.% of each element was substituted into the HA structure. The best condition of sintering temperature for Sr/B/S-HA was 1100°C for 10 hrs due to the resulting small grain size, improved cell adhesion and more collagen and osteocalcin production. These results suggest that the substitution of elements into the HA structure can provide novel bioceramics for control of physical mechanical and cell responses properties.
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Li, Bo. "The role of BK channel in cellular proliferation and differentiation in human osteoblast and osteoblast-like cells." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/35876/.

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Both excitable and non-excitable cells possess plasma membrane ion channels and evidence has accumulated over the last 30 or so years that these channels perhaps play key roles in the cell life and death. This Thesis investigated the characteristics and putative functions of one class of potassium channel, the BK channel in osteoblast-like cells and primary osteoblasts from human, rat and mouse. The properties and functions were defined in vitro using a combination of patch-clamp, reverse transcription-polymerase chain reaction (RT-PCR) and functional assays for cell growth and mineralisation. RT-PCR showed the presence of KCNMA1, KCNMB1, KCNMB2, KCNMB3 and KCNMB4, the gene for BK channel α, β1, β2, β3 and β4 subunits respectively. The channel was voltage-dependent with a mean unitary conductance of 315 pS in cell-attached patches, a conductance of 124 pS in excised outside-out and 151 pS in inside-out patches. The channel was blocked by TEA (0.3 mM), TBuA (1 mM), TPeA (1-10 μM), THeA (1-3 μM), tetrandrine (5-30 μM) and paxilline (10 μM) and was activated by isopimaric acid (20 μM). Notably iberiotoxin (IbTX) (90 nM) only blocked a proportion of the channels tested (2/5). Osteoblast-like MG63 cell number changed in response to BK channel modulators. It increased significantly with TEA and tetrandrine at low concentrations (1 mM, 3 μM respectively), and reduced at high concentrations (>10 mM, >10 μM respectively). It was not affected by IbTX (20-300 nM) or slotoxin (300 nM). The increase in cell number by TEA was blocked by isopimaric acid. In addition, TPeA and THeA caused a decrease of osteoblast-like SaOS2 cell mineralisation at the concentrations (3 and 0.3 μM, respectively) increased MG63 cell numbers. The BK channel has a distinctive pharmacology and represents a new target for therapeutic strategies in modulating osteoblast proliferation.
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Park, Jung Hwa. "The role of surface chemistry and wettability of microtextured titanium surfaces in osteoblast differentiation." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/44732.

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Biomaterial surface energy, chemical composition, charge, wettability and roughness all play an important role in determining the degree of the direct bone-to-implant interface, termed osseointegration. Surface chemistry, which is influenced by surface energy, wettability, and composition, is another factor that determines osteoblast phenotype and regulates osteoblast maturation. Increased surface energy is desirable for bone implants due to enhanced interaction between the implant surface and the biological environment. The extent of bone formation in vivo is also increased with increasing water wettability of implants. The physiological role of implant surface chemistry is important in determining the success of implant osseointegration because of molecular rearrangements, surface reactions, contamination, and release of toxic or biologically active ions that are determined by the starting chemistry. However, the role of surface chemistry on osteoblast response is not fully studied. Therefore, the overall goal of this dissertation is to understand how the surface chemistry, including wettability, chemical composition, and charge density, of titanium biomaterials impacts osteoblast maturation (in vitro). This study focuses on the general hypothesis that modifications of surface chemistry of titanium surfaces with sterilization or polyelectrolyte coating on titanium surfaces regulate osteoblast response.
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Huesa, Carmen. "Mechanotransduction in cells of the osteoblast lineage." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25468.

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Allen, Matthew Robert. "Mechanisms of impaired osteoblast function during disuse." Diss., Texas A&M University, 2003. http://hdl.handle.net/1969.1/1056.

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Prolonged periods of non-weightbearing activity result in a significant loss of bone mass which increases the risk of fracture with the initiation of mechanical loading. The loss of bone mass is partially driven by declines in bone formation yet the mechanisms responsible for this decline are unclear. To investigate the limitations of osteoblasts during disuse, marrow ablation was superimposed on hindlimb unloaded mice. Marrow ablation is a useful model to study osteoblast functionality as new cancellous bone is rapidly formed throughout the marrow of a long bone while hindlimb unloading is the most common method used to produce skeletal unloading. The specific hypotheses of this study were aimed at determining if changes in osteoblast functionality, differentiation, and/or proliferation were compromised in non-weightbearing bone in response to a bone formation stimulus. Additionally, the influence of having compromised osteoblast functionality at the time of stimulation was assessed in non-weightbearing bones. Key outcome measures used to address these hypotheses included static and dynamic cancellous bone histomorphometry, bone densitometry, and real-time polymerase chain reaction (PCR) analyses of gene expression. The results document similar ablation-induced increases of cancellous bone in both weightbearing and unloaded animals. Similarly, there was no influence of load on ablation-induced increases in cancellous bone forming surface or mineral apposition rate. Unloading did significantly attenuate the ablation-induced increase in bone formation rate, due to reduced levels of total surface mineralization. When osteoblast functionality was compromised prior to marrow ablation, bone formation rate increases were also attenuated in ablated animals due to reduced mineralization. Additionally, increases in forming surface were attenuated as compared to unloaded animals having normal osteoblast function at the time of ablation. Collectively, these data identify mineralization as the limiting step in new bone formation during periods of disuse. The caveat, however, is that when bone formation is stimulated after a period of unloading sufficient to compromise osteoblast functionality, increases in osteoblast recruitment to the bone surface are compromised.
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Books on the topic "Osteoblast"

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Najafova, Zeynab. Epigenetic regulation of osteoblast differentiation. Göttingen: Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017.

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Knight, Susan Mary. A study of osteoblast function in osteoporosis. Birmingham: University of Birmingham, 1994.

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Tarrant, Sarah Fiona. Osteoblast interactions with bone biomaterials 'in vitro'. Birmingham: Universityof Birmingham, 1989.

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Liu, Fina. Molecular and cellular analysis of the osteoblast lineage. [Toronto: University of Toronto, Faculty of Dentistry], 1997.

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Al-Ajmi, Nada Mohammad Zaid. The effect of clinostat rotation on osteoblast behaviour. Manchester: University of Manchester, 1997.

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Horgan, Fergal G. Osteoblast response to sputter deposited calcium phosphate thin film coatings. [S.l: The author], 2004.

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Steven, Doty, and United States. National Aeronautics and Space Administration., eds. Effects of hypogravity on osteoblast differentiation: Final report, NCC 2-846. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Perry, Judith Louise. Production and characterisation of monoclonal antibodies to rat osteoblast-like cells. Birmingham: University of Birmingham, 1989.

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Phillips, John L. Regulation of cytokine production in the rat osteoblast by tansforming growth factor-BETA. [s.l: s.l.], 1992.

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Turksen, Kursad. Analysis of the osteoblast lineage: Use of a cell culture model and monoclonal antibodies. [S.l.]: K. Turksen, 1991.

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Book chapters on the topic "Osteoblast"

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Baum, H. "Osteoblast." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_2317-1.

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Baum, H. "Osteoblast." In Springer Reference Medizin, 1797. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2317.

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Orriss, Isabel R., Sarah E. B. Taylor, and Timothy R. Arnett. "Rat Osteoblast Cultures." In Methods in Molecular Biology, 31–41. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-415-5_3.

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Dillon, Jane P., Victoria J. Waring-Green, Adam M. Taylor, Peter J. M. Wilson, Mark Birch, Alison Gartland, and James A. Gallagher. "Primary Human Osteoblast Cultures." In Methods in Molecular Biology, 3–18. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-415-5_1.

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Marie, Pierre J., and Pierre J. Marie. "Osteoblast Biology and Mechanosensing." In Mechanosensing Biology, 105–26. Tokyo: Springer Japan, 2011. http://dx.doi.org/10.1007/978-4-431-89757-6_8.

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Bukka, Prasanna, Marc D. McKee, and Andrew C. Karaplis. "Molecular Regulation of Osteoblast Differentiation." In Bone Formation, 1–17. London: Springer London, 2004. http://dx.doi.org/10.1007/978-1-4471-3777-1_1.

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Vrahnas, Christina, and Natalie A. Sims. "Basic Aspects of Osteoblast Function." In Osteoporosis, 1–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-69287-6_1.

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Arumugam, Meera Q., Roger A. Brooks, Neil Rushton, and William Bonfield. "Incorporation of Human Osteoblast Cells and Osteoblast-Like Cells into Porous Hydroxyapatite Scaffolds." In Bioceramics 17, 627–30. Stafa: Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-961-x.627.

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Chiba, Mirei, Ryosuke Miyai, and Haruhide Hayashi. "Micro-spatial Environment and Osteoblast Osteogenesis." In Interface Oral Health Science 2011, 110–11. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54070-0_23.

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de Gorter, David J. J., and Peter ten Dijke. "Signal Transduction Cascades Controlling Osteoblast Differentiation." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 15–24. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch2.

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Conference papers on the topic "Osteoblast"

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Tuan, Rocky S. "Functional Analysis of Bone-Biomaterial Interface." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2675.

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Abstract Proper function and long-term stability of orthopaedic implants depend on the intimate association between bone cells and the implant biomaterial, a process known as osseointegration. Understanding the processes responsible for the establishment and maintenance of a functional bone-biomaterial interface and how these processes may be enhanced is crucial to the rational design and optimization of prosthetic devices. We have utilized cellular, molecular, and high-resolution imaging approaches to analyze the mechanistic basis of bone-biomaterial interactions. Specifically, we have characterized the initial adhesion of osteoblasts in terms of kinetics and relationship to the surface topography and chemistry of the biomaterials, particularly the cobalt-chrome and titanium alloys commonly used to fabricate orthopaedic prostheses. Results from these studies indicate that the long-term performance of osteoblasts adherent to biomaterials is crucially dependent on the characteristics of the initial adhesion step. Furthermore, osteoactive factors such as members of the transforming growth factor-β superfamily, including TGF-β1 and BMP-2, significantly enhance osteoblast cell adhesion. The molecular components responsible for the adhesion process include extracellular matrix proteins (e.g. fibronectin and collagen type I) and their cognate membrane receptors, the integrins. Our recent studies reveal that specific downstream, intracellular signaling events are also activated as a result of osteoblast adhesion, and that these signaling events are coupled to signal transduction mechanisms mediating growth factor activity. These events in combination regulate the continued expression and maintenance of the osteoblastic phenotype of the adherent cells, resulting in matrix maturation and mineralization, hallmarks of the bony tissue. Our current efforts focus on defining the target molecular pathways responsible for bone cell functioning on biomaterials, and the identification of critical biological and material parameters to optimize long-term osteoblast function and interaction with orthopaedically relevant biomaterials. The information gathered from these studies should provide a rational basis for the design of optimal implant biomaterials. (Supported in part by the NIH and the Annenberg Foundation)
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Legoux, J. G., F. Chellat, R. S. Lima, B. R. Marple, M. N. Bureau, H. Shen, and G. A. Candeliere. "Development of Osteoblast Colonies on New Bioactive Coatings." In ITSC2006, edited by B. R. Marple, M. M. Hyland, Y. C. Lau, R. S. Lima, and J. Voyer. ASM International, 2006. http://dx.doi.org/10.31399/asm.cp.itsc2006p0059.

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Abstract The aging baby boomer population coupled with an increase in life expectancy is leading to a rising number of active elderly persons in occidental countries. As a result, the orthopedic implant industry is facing numerous challenges such as the need to extend implant life, reduce the incidence of revision surgery and improve implant performance. This paper reports results of an investigation on the bioperformance of newly developed coating-substrate systems. Hydroxyapatite (HA) and nano-titania (nano-TiO2) coatings were produced on Ti-6Al-4V and fiber reinforced polymer composite substrates. In vitro studies were conducted in order to determine the capacity of bioactive coatings developed to sustain osteoblast cells (fetal rat calvaria) adherence, growth and differentiation. As revealed by SEM observations and alkaline phosphatase activity (ALP), cell adhesion and proliferation demonstrated that HA coatings over a polymer composite are at least as good as HA coatings made over Ti-6Al-4V substrate in terms of osteoblast cell activity. Nano-TiO2 coatings produced by high-velocity oxy fuel (HVOF) spraying led to different results. For short term cell culture (4.5 and 24 hrs), the osteoblasts appeared more flattened when grown on nano-TiO2 than on HA. The surface cell coverage after 7 days of incubation was also more complete on nano-TiO2 than HA. Preliminary results indicate that osteoblast activity after 15 days of incubation on nano-TiO2 is equivalent to or greater than that observed on HA.
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Cox, Lieke G. E., Corrinus C. van Donkelaar, Bert van Rietbergen, Rik Huiskes, and Keita Ito. "Osteocytes in Bone Can Regulate the Turnover of Adjacent Mineralized Growth Plate Cartilage." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206251.

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It is generally believed that bone remodeling is controlled by osteocytes, which act as mechanosensors and regulate the activity of osteoblast and osteoclast cells [1,2]. Osteocytes seem suitable for this function, since they are the most abundant cell type of bone and they form an extensive network of cellular processes by gap junction connections to each other, lining cells, and osteoblasts [1,3].
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Shiraishi, Toshihiko, Kazuhiro Sakata, Shin Morishita, and Ryohei Takeuchi. "Visualization of Actin Fibers in a Living Osteoblast Under Shear Deformation." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39810.

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Bone cells are adaptive to surrounding mechanical conditions. Osteoblasts, one of bone cells, have been reported to be sensible to mechanical stimulation and change the generated bone mass. Activation of the signaling molecules in relation to the initial mechanoreception appears to be mediated though changes in the cytoskeleton. In this study, we propose a method to visualize cytoskeletal actin fibers in a living osteoblast under applied shear deformation and measure the local deformation of actin fibers. Transfection of MC3T3-E1, which is an osteoblast-like cell line, with GFP-actin was performed using a transfection reagent. Shear deformation was applied to the cell using a micropipette. As a result of the experiment, it is shown to be able to recognize the specific points such as points crossed by the actin fibers and obtain the local deformation vectors of the actin fiber network at the specific points in the cell. The present method contributes to not only obtaining the deformation distribution of actin fibers in cells but also understanding the mechanotransduction mechanisms.
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Zhang, Wenting, Yexin Gu, Qiaoling Sun, David S. Siegel, Peter Tolias, Zheng Yang, Woo Lee, and Jenny Zilberberg. "Abstract 344: Downregulation of osteoblastic N-cadherin decreases primary multiple myeloma cell - osteoblast interactions." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-344.

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Song, Wang, Yang Yueqin, and Chen Guoqing. "Effect of mechanical stress on formation of osteoblast in vitro — A new way to culture osteoblasts." In 2009 ISECS International Colloquium on Computing, Communication, Control, and Management (CCCM). IEEE, 2009. http://dx.doi.org/10.1109/cccm.2009.5267860.

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Van Dyke, William S., Ozan Akkus, and Eric Nauman. "Murine Osteochondral Stem Cells Express Collagen Type I More Strongly on PDMS Substrates Than on Tissue Culture Plastic." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14272.

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The discovery of the multipotent lineage of mesenchymal stem cells has dawned a new age in tissue engineering, where an autologous cell-seeded scaffold can be implanted into different therapeutic sites. Mesenchymal stem cells have been reported to differentiate into numerous anchorage-dependent cell phenotypes, including neurons, adipocytes, myoblasts, chondrocytes, tenocytes, and osteoblasts. A seminal work detailing that mesenchymal stem cells can be directed towards differentiation of different cell types by substrate stiffness alone [1] has led to numerous studies attempting to understand how cells can sense the stiffness of their substrate [2–3] Substrate stiffness has been shown to be an inducer of stem cell differentiation. MSCs on extremely soft substrates (250 Pa), similar to the stiffness of bone marrow, became quiescent but still retained their multipotency [4]. Elastic substrates in the stiffness range of 34 kPa revealed MSCs with osteoblast morphology, and osteocalcin along with other osteoblast markers were expressed [1]. However, osteogenesis has been found to increase on much stiffer (20–80 kPa) [5–6] (400 kPa) [7] as well as much softer substrates (75 Pa) [8]. Overall, cells have increased projected cell area and proliferation on stiffer substrates, leading to higher stress fiber formation. This study seeks to understand if the stiffness of the substrate has any effect on the differentiation potential of osteochondral progenitor cells into bone cells, using an in vitro dual fluorescent mouse model.
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Uemura, Toshimasa, Atsuko Nemoto, Jing An, Yin-kun Liu, Takafumi Yoshikawa, Hajime Ohgushi, Yoshinori Kuboki, Takashi Ushida, and Tetsuya Tateishi. "OSTEOPONTIN INVOLVEMENT IN OSTEOBLAST DIFFERENTIATION AND ITS EFFECT ON IN VIVO OSTEOGENIC POTENTIAL OF BONE MARROW DERIVED OSTEOBLASTS." In Proceedings of the 12th International Symposium on Ceramics in Medicine. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814291064_0064.

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Lima, R. S., B. R. Marple, H. Li, and K. A. Khor. "Biocompatible Nanostructured High Velocity Oxy-Fuel (HVOF) Sprayed Titania Coating." In ITSC2006, edited by B. R. Marple, M. M. Hyland, Y. C. Lau, R. S. Lima, and J. Voyer. ASM International, 2006. http://dx.doi.org/10.31399/asm.cp.itsc2006p0041.

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Abstract Nanostructured titania (TiO2) coatings were produced by high velocity oxy-fuel (HVOF) spraying. They were engineered as a possible candidate to replace hydroxyapatite (HA) coatings produced by air plasma spray (APS) on implants. They exhibited mechanical properties, such as hardness and bond strength, much superior to those of APS HA coatings. In addition to these characteristics, the surface of the nanostructured coatings exhibited regions with nanotextured features originating from the semi-molten nanostructured feedstock particles. This nanotexture is considered an asset, due to its better interaction with the adhesion proteins of the osteoblast cells, such as fibronectin, which exhibit dimensions in the order of nanometers. Osteoblast cell culture demonstrated that this type of coating supported osteoblast cell growth and did not negatively affect cell viability.
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Yupeng Chen and Thomas J. Webster. "Improving osteoblast growth through BMP-7 short peptides." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413373.

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Reports on the topic "Osteoblast"

1

Mercer, Robyn R. Breast Cancer Metastasis to Bone Affects Osteoblast Differentiation. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada426273.

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Mercer, Robyn R., and Andrea M. Mastro. Breast Cancer Metastasis to Bone Affects Osteoblast Differentiation. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416623.

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Karaplis, Andrew. Osteoblast-Derived PTHRP and Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada625302.

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Navone, Nora M. Osteoblast-Prostate Cancer Cell Interaction in Prostate Cancer Bone. Fort Belvoir, VA: Defense Technical Information Center, February 2000. http://dx.doi.org/10.21236/ada391088.

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Paranavitana, Chrysanthi. In Vitro Osteoblast Model for Bone Wound Infections and Antimicrobial Therapy. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada608594.

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Sanders, Jennifer L. Actions of Tamoxifen and Estrogen on Osteoblast Protein Kinase C Expression. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada306529.

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Bussard, Karen M. The Role of Osteoblast-Derived Cytokines in Bone Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada471009.

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Bussard, Karen M. The Role of Osteoblast-Derived Inflammatory Cytokines in Bone Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada485641.

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Wiren, Kristine M., and Karl Jepsen. Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality, and Bone Architecture. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada448583.

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Wiren, Kristine M., and Russell Turner. Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality and Bone Architecture. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada524383.

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