Academic literature on the topic 'Osteogenic Markers'
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Journal articles on the topic "Osteogenic Markers"
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Wang, Jing, Junyi Liao, Fugui Zhang, Dongzhe Song, Minpeng Lu, Jianxiang Liu, Qiang Wei, et al. "NEL-Like Molecule-1 (Nell1) Is Regulated by Bone Morphogenetic Protein 9 (BMP9) and Potentiates BMP9-Induced Osteogenic Differentiation at the Expense of Adipogenesis in Mesenchymal Stem Cells." Cellular Physiology and Biochemistry 41, no. 2 (2017): 484–500. http://dx.doi.org/10.1159/000456885.
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Background: BMP9 induces both osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs). Nell1 is a secretory glycoprotein with osteoinductive and anti-adipogenic activities. We investigated the role of Nell1 in BMP9-induced osteogenesis and adipogenesis in MSCs. Methods: Previously characterized MSCs iMEFs were used. Overexpression of BMP9 and NELL1 or silencing of mouse Nell1 was mediated by adenoviral vectors. Early and late osteogenic and adipogenic markers were assessed by staining techniques and qPCR analysis. In vivo activity was assessed in an ectopic bone formation model of athymic mice. Results: We demonstrate that Nell1 expression was up-regulated by BMP9. Exogenous Nell1 potentiated BMP9-induced late stage osteogenic differentiation while inhibiting the early osteogenic marker. Forced Nell1 expression enhanced BMP9-induced osteogenic regulators/markers and inhibited BMP9-upregulated expression of adipogenic regulators/markers in MSCs. In vivo ectopic bone formation assay showed that exogenous Nell1 expression enhanced mineralization and maturity of BMP9-induced bone formation, while inhibiting BMP9-induced adipogenesis. Conversely, silencing Nell1 expression in BMP9-stimulated MSCs led to forming immature chondroid-like matrix. Conclusion: Our findings indicate that Nell1 can be up-regulated by BMP9, which in turn accelerates and augments BMP9-induced osteogenesis. Exogenous Nell1 may be exploited to enhance BMP9-induced bone formation while overcoming BMP9-induced adipogenesis in regenerative medicine.
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Choi, Somang, Sung Hyun Noh, Chae Ouk Lim, Hak-Jun Kim, Han-Saem Jo, Ji Seon Min, Kyeongsoon Park, and Sung Eun Kim. "Icariin-Functionalized Nanodiamonds to Enhance Osteogenic Capacity In Vitro." Nanomaterials 10, no. 10 (October 20, 2020): 2071. http://dx.doi.org/10.3390/nano10102071.
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Nanodiamonds (NDs) have been used as drug delivery vehicles due to their low toxicity and biocompatibility. Recently, it has been reported that NDs have also osteogenic differentiation capacity. However, their capacity using NDs alone is not enough. To significantly improve their osteogenic activity, we developed icariin (ICA)-functionalized NDs (ICA-NDs) and evaluated whether ICA-NDs enhance their in vitro osteogenic capacity. Unmodified NDs and ICA-NDs showed nanosized particles that were spherical in shape. The ICA-NDs achieved a prolonged ICA release for up to 4 weeks. The osteogenic capacities of NDs, ICA (10 μg)-NDs, and ICA (50 μg)-NDs were demonstrated by alkaline phosphatase (ALP) activity; calcium content; and mRNA gene levels of osteogenic-related markers, including ALP, runt-related transcript factor 2 (RUNX2), collagen type I alpha 1 (COL1A1), and osteopontin (OPN). In vitro cell studies revealed that ICA (50 μg)-ND-treated MC3T3-E1 cells greatly increased osteogenic markers, including ALP, calcium content, and mRNA gene levels of osteogenic-related markers, including ALP, RUNX2, COL1A1, and OPN compared to ICA (10 μg)-NDs or ND-treated cells. These our data suggest that ICA-NDs can promote osteogenic capacity.
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Zhang, Fei, Zehua Zhang, Dong Sun, Shiwu Dong, Jianzhong Xu, and Fei Dai. "Periostin: A Downstream Mediator of EphB4-Induced Osteogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/7241829.
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Erythropoietin-producing hepatocyte B4 (EphB4) has been reported to be a key molecular switch in the regulation of bone homeostasis, but the underlying mechanism remains poorly understood. In this study, we investigated the role of EphB4 in regulating the expression of periostin (POSTN) within bone marrow-derived mesenchymal stem cells (MSCs) and assessed its effect and molecular mechanism of osteogenic induction in vitro. Treatment with ephrinB2-FC significantly increased the expression of POSTN in MSCs, and the inhibition of EphB4 could abrogate this effect. In addition, osteogenic markers were upregulated especially in MSCs overexpressing EphB4. To elucidate the underlying mechanism of cross talk between EphB4 and the Wnt pathway, we detected the change in protein expression of phosphorylated-glycogen synthase kinase 3β-serine 9 (p-GSK-3β-Ser9) andβ-catenin, as well as the osteogenic markers Runx2 and COL1. The results showed that GSK-3βactivation and osteogenic marker expression levels were downregulated by ephrinB2-FC treatment, but these effects were inhibited by blocking integrinαvβ3 in MSCs. Our findings demonstrate that EphB4 can promote osteogenic differentiation of MSCs via upregulation of POSTN expression. It not only helps to reveal the interaction mechanism between EphB4 and Wnt pathway but also brings a better understanding of EphB4/ephrinB2 signaling in bone homeostasis.
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Di Pietro, Lorena, Marta Barba, Chiara Prampolini, Sabrina Ceccariglia, Paolo Frassanito, Alessia Vita, Enrico Guadagni, et al. "GLI1 and AXIN2 Are Distinctive Markers of Human Calvarial Mesenchymal Stromal Cells in Nonsyndromic Craniosynostosis." International Journal of Molecular Sciences 21, no. 12 (June 19, 2020): 4356. http://dx.doi.org/10.3390/ijms21124356.
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All skeletal bones house osteogenic stem cell niches, in which mesenchymal stromal cells (MSC) provide progenitors for tissue growth and regeneration. They have been widely studied in long bones formed through endochondral ossification. Limited information is available on the composition of the osteogenic niche in flat bones (i.e., skull vault bones) that develop through direct membranous ossification. Craniosynostosis (CS) is a congenital craniofacial defect due to the excessive and premature ossification of skull vault sutures. This study aimed at analysing the expression of GLI1, AXIN2 and THY1 in the context of the human skull vault, using nonsyndromic forms of CS (NCS) as a model to test their functional implication in the aberrant osteogenic process. The expression of selected markers was studied in NCS patients’ calvarial bone specimens, to assess the in vivo location of cells, and in MSC isolated thereof. The marker expression profile was analysed during in vitro osteogenic differentiation to validate the functional implication. Our results show that GLI1 and AXIN2 are expressed in periosteal and endosteal locations within the osteogenic niche of human calvarial bones. Their expression is higher in MSC isolated from calvarial bones than in those isolated from long bones and tends to decrease upon osteogenic commitment and differentiation. In particular, AXIN2 expression was lower in cells isolated from prematurely fused sutures than in those derived from patent sutures of NCS patients. This suggests that AXIN2 could reasonably represent a marker for the stem cell population that undergoes depletion during the premature ossification process occurring in CS.
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Chen, Kai, Xianqi Li, Ni Li, Hongwei Dong, Yiming Zhang, Michiko Yoshizawa, and Hideaki Kagami. "Spontaneously Formed Spheroids from Mouse Compact Bone-Derived Cells Retain Highly Potent Stem Cells with Enhanced Differentiation Capability." Stem Cells International 2019 (May 5, 2019): 1–13. http://dx.doi.org/10.1155/2019/8469012.
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The results from our recent study showed the presence of two distinct spheroid-forming mechanisms, i.e., spontaneous and mechanical. In this study, we focused on the spontaneously formed spheroids, and the character of spontaneously formed spheroids from mouse compact bone-derived cells (CBDCs) was explored. Cells from (C57BL/6J) mouse leg bones were isolated, and compact bone-derived cells were cultured after enzymatic digestion. Spontaneous spheroid formation was achieved on a culture plate with specific water contact angle as reported. The expression levels of embryonic stem cell markers were analyzed using immunofluorescence and quantitative reverse transcription polymerase chain reaction. Then, the cells from spheroids were induced into osteogenic and neurogenic lineages. The spontaneously formed spheroids from CBDCs were positive for ES cell markers such as SSEA1, Sox2, Oct4, and Nanog. Additionally, the expressions of fucosyltransferase 4/FUT4 (SSEA1), Sox2, and Nanog were significantly higher than those in monolayer cultured cells. The gene expression of mesenchymal stem cell markers was almost identical in both spheroids and monolayer-cultured cells, but the expression of Sca-1 was higher in spheroids. Spheroid-derived cells showed significantly higher osteogenic and neurogenic marker expression than monolayer-cultured cells after induction. Spontaneously formed spheroids expressed stem cell markers and showed enhanced osteogenic and neurogenic differentiation capabilities than cells from the conventional monolayer culture, which supports the superior stemness.
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Gu, Mingyong, and Runquan Zheng. "Apolipoprotein E Inhibits Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells by Inhibiting β-Catenin Expression." Journal of Biomaterials and Tissue Engineering 9, no. 12 (December 1, 2019): 1739–44. http://dx.doi.org/10.1166/jbt.2019.2194.
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Bone marrow mesenchymal stem cells (BMSCs) can differentiate into adipocytes, osteoblasts. Apolipoprotein E (ApoE) is closely related to bone metabolism and its effect on bone marrow mesenchymal stem cells is unclear. Therefore, this study investigated ApoE's effect on BMSCs osteogenic differentiation. BMSCs were isolated from ApoE – and WT mouse and cultured to induce osteogenic induction followed by analysis of expression of osteogenic differentiation marker genes by Real-time PCR, calcium nodules formation by ARS staining, ALP activity and -catenin protein level by Western blot. The number of bone differentiation markers, ALP activity and calcium nodules formation as well as β-catenin protein level in ApoE– group were significantly elevated compared with WT (P < 0 05). After treatment with DKK-1, β-catenin expression was significantly reduced (P < 0 05) without difference between ApoE– + DKK-1 group and WT group (P > 0 05). WT+ DKK1 group showed significantly reduced osteogenic differentiation marker expression, ALP activity and calcium nodule number compared to WT (P < 0 05) without difference between ApoE– + DKK1 group and WT group (P > 0 05). ApoE inhibits BMSCs osteogenic differentiation by inhibiting β-catenin expression.
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Li, Xiaoliang, Guofeng Xia, Hongmei Xin, Chunsheng Tao, Weiwei Lai, and Peifeng Sun. "lncRNA MALAT1 Inhibits Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells by Down-Regulating WNT5A." Journal of Biomaterials and Tissue Engineering 9, no. 11 (November 1, 2019): 1520–27. http://dx.doi.org/10.1166/jbt.2019.2167.
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ncRNA involves in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). WNT5A participates in the growth and development of osteogenic differentiation. This study aims to investigate whether lncRNA MALAT1 regulates BMSCs osteogenesis through WNT5A. qRT-PCR was done to detect the lncRNA MALAT1 level and osteogenic markers in osteoporosis patients and control groups. The above markers and WNT5A protein levels were detected by Western blot. The degree of osteogenic differentiation was detected by ALP activity assay and ALP staining. The differentiation ability of BMSCs after lncRNA MALAT1 overexpression was detected by ARS staining. The binding site of lncRNA MALAT1 to WNT5A was determined by dual luciferase reporter assay. lncRNA MALAT1 expression was higher in patients with osteoporosis, and decreased significantly with increased osteogenic induction. Overexpression of lncRNA MALAT1 in BMSCS reduced WNT5A level, while interference with lncRNA MALAT1 increased WNT5A levels. In cells with overexpression of lncRNA MALAT1, transfection of si-WNT5A can significantly downregulate the RUNX2, OSX, ALP, OCN, OPN, and COL1A1, thereby inhibiting osteogenic differentiation, interfering with the regulation of WNT signaling pathway and regulating BMSCs osteogenic differentiation. lncRNA MALAT1 and WNT5A can regulate BMSCs osteogenesis, thus accelerating the progression of osteoporosis.
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Kannan, Sangeetha, Jyotirmoy Ghosh, and Sujoy K. Dhara. "Osteogenic differentiation potential of porcine bone marrow mesenchymal stem cell subpopulations selected in different basal media." Biology Open 9, no. 10 (September 24, 2020): bio053280. http://dx.doi.org/10.1242/bio.053280.
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ABSTRACTMultipotent porcine mesenchymal stem cells (pMSC) are invaluable for research and therapeutic use in regenerative medicine. Media used for derivation and expansion of pMSC may play an important role for the selection of MSC subpopulation at an early stage and thereby, the specific basal medium may also affect differentiation potential of these cells. The present study was undertaken to evaluate the effects of αMEM, aDMEM, M199, αMEM/M199, aDMEM/M199 and αMEM/aDMEM media on (1) porcine bone marrow MSC derivation; (2) expression of number of osteogenic markers (ALP, COL1A1, SPP1 and BGLAP) at 5th and 10th passage in pMSC before differentiation; and (3) differentiation of pMSC (at 5th passage) to osteogenic lineage. Morphological changes and matrix formation in osteogenic cells were evaluated by microscopic examination. Calcium deposits in osteocytes were confirmed by Alizarin Red S staining. Based on expression of different markers, it was evident that selection of bone marrow pMSC subpopulations was independent of basal media used. However, the differentiation of those pMSCs, specifically to osteogenic lineage, was dependent on the medium used for expansion of pMSC at the pre-differentiation stage. We demonstrated here that the pMSC grown in combined αMEM/aDMEM (1:1) medium expressed number of osteogenic markers and these pMSC underwent osteogenic differentiation most efficiently, in comparison to porcine mesenchymal stem cells grown in other media. In conclusion, osteogenic differentiation potential of pMSC maintained in αMEM/aDMEM medium was observed significantly higher compared to cells cultivated in other media and therefore, the combined medium αMEM/aDMEM (1:1) may preferentially be used for expansion of pMSC, if needed for osteogenic differentiation.
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Wang, Jian, Bo Xiang, Jixian Deng, Darren H. Freed, Rakesh C. Arora, and Ganghong Tian. "Inhibition of Viability, Proliferation, Cytokines Secretion, Surface Antigen Expression, and Adipogenic and Osteogenic Differentiation of Adipose-Derived Stem Cells by Seven-Day Exposure to 0.5 T Static Magnetic Fields." Stem Cells International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/7168175.
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After seven-day exposure to 0.5-Tesla Static Magnetic Field (SMF), Adipose-derived Stem Cells (ASCs) and those labeled by superparamagnetic iron oxide (SPIO) nanoparticles were examined for viability by methyl thiazol tetrazolium (MTT) assay, proliferation by cell counting and bromodeoxyuridine (BrdU) incorporation, DNA integrity by single cell gel electrophoresis, surface antigen by flow cytometry analysis, and the expression of cytokines and genetic markers by reverse transcription-PCR and underwent adipogenic and osteogenic differentiation assessed by quantifying related specific genes expression. The SMF slightly reduced cell viability and proliferation and inhibited the expression of CD49d, CD54, and CD73 but did not damage DNA integrity. The SMF slightly downregulated the expression of cytokines including Vascular Endothelial Growth Factor (VEGF), Insulin-like Growth Factor-1 (IGF-1), Transforming Growth Factor Beta 1 (TGF-β1), genetic markers comprising Stem Cell Antigen-1 (Sca1), Octamer-4 (Oct-4), ATP-binding Cassette Subfamily B Member 1 (ABCB1), adipogenic marker genes containing Lipoprotein Lipase (LPL), Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ), and osteogenic marker genes including Secreted Phosphor-protein 1 (SPP1) and Osterix (OSX). Exposure to 0.5 T SMF for seven days inhibited viability, proliferation, surface antigen expression, cytokine secretion, stem cell genetic marker expression, and adipogenic and osteogenic differentiation but did not affect the DNA integrity in ASCs with or without SPIO labeling.
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Zhang, Hongyu, Li Li, Qian Dong, Yufeng Wang, Qiaoling Feng, Xinying Ou, Pengfei Zhou, Tongchuan He, and Jinyong Luo. "Activation of PKA/CREB Signaling is Involved in BMP9-Induced Osteogenic Differentiation of Mesenchymal Stem Cells." Cellular Physiology and Biochemistry 37, no. 2 (2015): 548–62. http://dx.doi.org/10.1159/000430376.
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Background/Aims: BMP9 is highly capable of promoting osteogenic differentiation of mesenchymal stem cells (MSCs) although the molecular mechanism involved is largely unknown. Here, we explored the detail role of PKA/CREB signaling in BMP9-induced osteogenic differentiation. Methods: Activation status of PKA/CREB signaling is assessed by nonradioactive assay and Western blot. Using PKA inhibitors and a dominant negative protein of CREB (A-CREB), we investigated the effect of PKA/CREB signaling on BMP9-induced osteogenic differentiation. Results: We found that BMP9 promotes PKA activity and enhances CREB phosphorylation in MSCs. BMP9 is shown to down-regulate protein kinase A inhibitor γ (PKIγ) expression. We demonstrated that PKA inhibitors suppress BMP9-induced early osteogenic marker alkaline phosphatase (ALP) activity in MSCs as well as late osteogenic markers osteopontin (OPN), osteocalcin (OCN) and matrix mineralization. We found that PKA inhibitor reduces BMP9-induced Runx2 activation and p38 phosphorylation in MSCs. Lastly, interference of CREB function by A-CREB decreased BMP9-induced osteogenic differentiation as well. Conclusion: Our results revealed that BMP9 may activate PKA/CREB signaling in MSCs through suppression of PKIγ expression. It is noteworthy that inhibition of PKA/CREB signaling may impair BMP9-induced osteogenic differentiation of MSCs, implying that activation of PKA/CREB signaling is required for BMP9 osteoinductive activity.
Dissertations / Theses on the topic "Osteogenic Markers"
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Ishiy, Felipe Augusto André. "Evaluation of molecular markers in osteogenic differentiation of mesenchymal stem cells." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-20032017-104921/.
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The use of stem cells is a promising therapeutic approach for tissue engineering by their ability to boost tissue regeneration, and to model in vitro human genetics disorders since it provides continuous supplies of cells with differentiation potential. Our study has been focused in the identification of molecules or mechanisms that could contribute to a better osteogenesis in mesenchymal stem cells (MSC). To achieve our goals we have explored the osteopontential differences of stem cells from different sources. In this regard, we have observed that MSCs from human exfoliated deciduous teeth (SHED) presented higher in vitro osteogenic differentiation potential (OD) as compared to MSCs derived from human adipose tissue (hASCs). Through microarray analysis and cell sorting, we have shown that IGF2 and CD105 expression levels contribute to these osteopontential cell differences, that is, higher IGF2 expression levels and lower CD105 expression levels were associated with the increased osteogenic potential of SHED as compared to hASCs. The molecular mechanisms associated with the diferent expression levels of IGF2 and CD105 in these cells were also investigated. Despite the advantages of adult MSCs they can exhibit drawbacks such as restricted self-renewal and limited cell amounts. Induced Pluripotent Stem Cells (iPSC) technology has emerged as an alternative cell source, as they provide more homogeneous cellular populations with prolonged self-renewal and higher plasticity. We verified that the OD of MSC-like iPSC differs from MSCs and it depends on the iPSCs originating cellular source. Comparative in vitro osteogenesis analysis showed higher osteogenic potential in MSC-like cells derived from iPS-SHED when compared with MSC-like cells from iPS-FIB and SHED. iPSCs can be also used as a tool to model genetic disorders. We have thus proposed to verify if it could be possible to in vitro model Treacher-Collins syndrome, a condition with deficient craniofacial bone development. We have compared the effects of pathogenic mutations in TCOF1 gene in cell proliferation, differentiation potential between MSCs, dermal fibroblasts, neural-crest like and MSC-like cells differentiated from iPSCs.TCS cells showed changes in cell properties anddysregulated expression of chondrogenesis markers during osteogenic and chondrogenic differentiation. In summary, the comparative analysis of stem cells of different sources allow us to identify markers that may facilitate osteogenesis and that it is possible to establish an in vitro model to Treacher-Collins syndromeO uso de células-tronco trata-se de uma abordagem terapêutica promissora para a engenharia de tecidos, devido à sua capacidade na regeneração de tecidos, e para modelamento in vitro de distúrbios genéticos humanos, uma vez que fornece um abastecimento contínuo de células com potencial de diferenciação. Nosso estudo se propos a identificar moléculas e mecanismos que contribuem na otimização da osteogênese de células-tronco mesenquimais (MSCs). Para atingir nossos objetivos exploramos as diferenças no potencial osteogênico (PO) de MSCs de diferentes fontes. Observamos que MSCs de polpa de dente decíduo humano (SHED) apresentaram maior PO em comparação com as MSC derivadas de tecido adiposo humano (hASCs). Através de análise de microarray de expressão e cell sorting, demonstramos que os níveis de expressão de IGF2 e CD105 contribuem para as diferenças do PO, onde a maior expressão de IGF2 e menor expressão de CD105 estão associadas a maior PO em SHED quando comparado as hASCs. Também investigamos os mecanismos moleculares associados aos diferentes níveis de expressão de IGF2 E CD105 em ambas as fontes celulares. Apesar das vantagens, as MSCs podem apresentar pontos negativos como restrita auto-renovação e menor quantidade de células. Células-tronco pluripotentes induzidas (iPSC) surgem como uma fonte celular alternativa, proporcionando populações celulares homogêneas com auto-renovação prolongada e maior plasticidade. O PO de MSC-like iPSC difere de MSCs, e este potencial é dependente da fonte celular em que as iPSCs são obtidas. Análise comparativa de PO in vitro demonstrou maior osteogênse em células MSC-like derivadas de iPS-SHED quando comparada as células MSC-like de iPSCs-fibroblastos e SHED. iPSCs também podem ser utilizadas como ferramenta para investigar doenças genéticas humanas. Propomos a modelagem in vitro da síndrome de Treacher-Collins (TSC), doença que acomete as estruturas craniofaciais durante o desenvolvimento ósseo. Comparamos os efeitos de mutações patogênicas no gene TCOF1 na proliferação celular, potencial de diferenciação entre MSCs, fibroblastos dérmicos, neural-crest like e células MSC-like diferenciadas de iPSCs. Células de pacientes TCS exibiram alterações em propriedades celulares e na expressão de marcadores osteogênicos e condrogênicos. Em resumo, a análise comparativa de células-tronco de diferentes fontes permitiu a identificação de marcadores e mecanismos que podem facilitar a osteogênese e tambem demonstramos que é possível modelar in vitro a síndrome de Treacher-Collins
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Mansour, Ali. "Mécanismes physiopathologiques de la calcification vasculaire : les vésicules extracellulaires comme cible thérapeutique potentielle." Thesis, Amiens, 2020. http://www.theses.fr/2020AMIE0029.
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Les maladies cardiovasculaires (MCV) sont classées en tête de liste parmi les principales causes de décès dans le monde. La calcification de la paroi vasculaire entraîne diverses conséquences cardiovasculaires critiques et explique les taux de mortalité élevés chez les patients atteints de nombreuses maladies comme le diabète, l'athérosclérose et la maladie rénale chronique (IRC). VC est un processus actif avec des caractéristiques de la physiologie osseuse et il est régulé par des processus inductifs et inhibiteurs multifactoriels. Au cours du processus de calcification, les cellules musculaires lisses vasculaires (VSMC) subissent un processus ostéogénique actif pour devenir des cellules de type ostéoblaste et libérer des populations hétérogènes de Vésicules Extracellulaires (EV). Les VE agissent comme des foyers de nucléation pour la cristallisation grâce à leur interaction avec le collagène de type 1 (Col1) via les intégrines et leur teneur en protéines procalcifiantes soutient fortement la progression de la calcification. Parce que ces deux mécanismes sont cruciaux pour le développement de la VC, ils représentent finalement deux cibles thérapeutiques pour la régression de la VC. Notre objectif principal était d'identifier de nouvelles molécules naturelles ou synthétisées chimiquement pouvant inhiber la VC. Nous avons démontré la capacité d'un acide oligogalacturonique spécifique (DP8), extrait de graines de lin, à inhiber la calcification induite par Pi in vitro et ex vivo en diminuant l'expression des marqueurs ostéogéniques, masquant une répétition consensus des acides aminés trouvée dans Col1 (séquence: GFOGER) , et empêchant ainsi les VE de se lier. Nous avons également synthétisé chimiquement un peptide GFOGER et vérifié sa capacité à inhiber la calcification. Semblable à DP8, le peptide GFOGER a été capable d'inhiber la calcification induite par Pi in vitro et ex vivo en régulant à la baisse l'expression des marqueurs ostéogéniques et en modifiant la teneur en protéines des EV dérivés des VSMC. Par conséquent, nos travaux suggèrent deux nouvelles approches thérapeutiques pour la prévention de la CVCardiovascular diseases (CVDs) are classified on top of the list among different death leading causes in the world. Calcification of the vessel wall leads to various critical cardiovascular consequences and accounts for high mortality rates in patients with many diseases like diabetes, atherosclerosis and chronic kidney disease (CKD). VC is an active process with features of bone physiology and it is regulated by multifactorial inductive and inhibitory processes. During the calcification process, Vascular Smooth Muscle Cells (VSMCs) undergo active osteogenic process to become osteoblast-like cells and release heterogeneous populations of Extracellular Vesicles (EVs). EVs act as nucleating foci for crystallization through their interaction with type 1 collagen (Col1) via integrins and their procalcifying protein content strongly supports calcification progression. Because these two mechanisms are crucial for the development of VC, they eventually represent two therapeutic targets for VC regression. Our primary objective was to identify new natural or chemically synthesized molecules that can inhibit VC. We demonstrated the ability of a specific oligogalacturonic acid (DP8), extracted from flax seeds, to inhibit in vitro and ex-vivo Pi-induced calcification by diminishing osteogenic markers expression, masking a consensus amino acid repeat found in Col1 (sequence: GFOGER), and thus preventing EVs from binding. Also we chemically synthesized a GFOGER peptide and checked its ability to inhibit calcification. Similar to DP8, GFOGER peptide was able to inhibit in vitro and ex-vivo Pi-induced calcification by downregulating osteogenic markers expression and through modifying the protein content of VSMCs derived EVs. Therefore, our work suggests two novel therapeutic approaches for the prevention of VC
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Yew, Tu-Lai, and 姚道禮. "Ex vivo targeting of p21Cip1/Waf1 enhances proliferation, the expression of stemness markers and osteogenic potential of human bone marrow-derived mesenchymal stem cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/05834285182497162280.
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博士國立陽明大學
口腔生物研究所
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Abstract Cell-based therapies using bone marrow-derived mesenchymal stem cells (MSCs) demonstrate great potential in bone regenerative therapies. Ex vivo expansion of MSCs is often required to generate adequate cell numbers in clinical applications. Senescence of MSCs occurs along with ex vivo passages and results in lower proliferation rate, loss of stemness and compromised therapeutic potential. However, currently no effective and safe method is available to solve the senescence problem. Previous studies indicated that a cell cycle regulator, p21, may be associated with cell senescence. We hypothesized that p21 may play an important role in the senescence of bone marrow-derived MSCs. The purpose of this research was to determine the role of p21 expression in the senescence of human bone marrow-derived MSCs. The results indicated that MSCs increased in p21 expression and became senescent along with ex vivo expansion. Lentiviral transduction of senescent MSCs with p21 shRNAs was able to increase their proliferation capacity, expression of stemness markers, and osteogenic potential in vitro. More importantly, the reduction of p21 expression enhanced the bone repair capacity of senescent MSCs in a mouse calvarial defect model. The p21-knockdowned MSCs showed increased telomerase activity and telomere length but maintained normal chromosome integrity and did not acquire tumorigenic potential. In conclusion, p21 plays an important role in senescence of human bone marrow-derived MSCs. The knockdown of p21 may become an effective and safe strategy to prevent or reduce the senescence of MSCs during ex vivo expansion.
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McKenzie, Kristen Penny. "CD31(-) HipOps - A Highly Osteogenic Cell Population From Mouse Bone Marrow." Thesis, 2012. http://hdl.handle.net/1807/33761.
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Multipotent mesenchymal stem cells (MSCs), found in many adult tissues, may be useful for regenerative medicine applications. Their identification and purification have been difficult due to their low frequency and lack of unambiguous markers. Using a magnetic micro-beads negative selection technique to remove contaminating hematopoietic cells from mouse bone marrow stromal cells (BMSCs), our lab recently isolated a highly purified osteoprogenitor (HipOp) population that was also enriched for other mesenchymal precursors, including MSCs (Itoh and Aubin, 2009). To further enhance enrichment, we positively selected BMSCs and HipOps for CD73, a putative MSC marker, which resulted in no significant additional enrichment for osteoprogenitors when the population was tested in vitro. However, we also found that HipOps were enriched in vascular endothelial cells, and that removing these cells by further negative selection with CD31/PECAM resulted in a CD31(-) HipOp population with higher osteogenic capacity than HipOps in vitro and in vivo.
Book chapters on the topic "Osteogenic Markers"
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Barthold, Mare, H. Mayer, and Volker Jäger. "Cultivation of Primary Osteogenic Cells in Serum-Reduced or Serum-Free Culture Media: Attachment, Proliferation and Differentiation." In Animal Cell Technology: From Target to Market, 581–83. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0369-8_139.
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Borer, Katarina T., Qingyun Zheng, Adam I. Daoud, Thomas Kernozek, Melissa M. Gross, and Blake J. Roessler. "Facilitation of Osteogenic Bone Marker Release in Postmenopausal Women by Single, Rather Than Spaced, Mechanical Loading or Anabolic Hormones." In TRANSLATIONAL - Bone, Calciotropic Hormones & Vitamin D, P2–108—P2–108. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p25.p2-108.
Full textConference papers on the topic "Osteogenic Markers"
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Chung, Eunna, and Marissa Nichole Rylander. "Multi-Stress Conditioning Can Synergisticly Enhance Production of Osteogenic Markers and Heat Shock Proteins." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19511.
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Tissue regeneration can be enhanced by introduction of biochemical and mechanical cues. We investigated the effect of thermal and mechanical stress alone or in combination with growth factors (GFs) (BMP-2 and TGF-β1) on cell proliferation and induction of heat shock proteins and bone-related proteins by MC3T3-E1mouse preosteoblasts. Thermal and mechanical stress conditioning alone induced bone-related proteins such as osteocalcin (OCN), vascular endothelial growth factor (VEGF), osteoprotegerin (OPG), and osteopontin (OPN) and heat shock proteins (HSP27, HSP47, HSP70). Cell proliferation was increased by cyclic tension in combination with growth factors. Combined thermal and mechanical stress induced synergistic expression of HSPs and VEGF. Therefore, utilization of thermal and tensile stress conditioning can stimulate bone healing or regeneration.
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Ren, Tingting, Sajida Piperdi, Amy Y. Park, and Richard Gorlick. "Abstract 1418: Screening and identification of key surface markers of mesenchymal stem cell osteogenic differentiation and osteosarcoma development." 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.am2015-1418.
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Chen, Joseph, Charles I. Fisher, M. K. Sewell-Loftin, and W. David Merryman. "Calcific Nodule Morphogenesis by Aortic Valve Interstitial Cells: Synergism of Applied Strain and TGF-β1." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53899.
Full textAbstract:
Calcific Aortic Valve Disease (CAVD) is the third most common cause of cardiovascular disease, affecting nearly 5 million people in the United States alone. It is now the most common form of acquired valvular disease in industrialized countries and will likely affect more individuals in the coming years as the prevalence increases with life expectancy. It is known that the progression of CAVD is closely related to the behavior of aortic valve interstitial cells (AVICs); however the cellular mechanobiological mechanisms leading to dysfunction remain unclear. Generally, CAVD is characterized by the formation of calcified AVIC aggregates with an apoptotic core. These aggregates increase the leaflet stiffness and impede normal valve function. Multiple studies have investigated the effects of various biochemical cues on this process, such as transformation growth factor β1 (TGF-β1), on the regulation of nodule formation [1]. Additionally, Yip et al revealed that matrix stiffness controls nodule formation in vitro, with stiffer substrates promoting apoptotic nodule formation, while compliant substrates generated nodules containing cells with osteoblast markers [2]. This suggests that matrix stiffness is involved in the regulatory mechanisms of nodule formation and may initiate different types of nodule formation (i.e. osteogenic vs. dystrophic). In the current study, we examined the synergistic role of strain and TGF-β1 in the generation of calcified nodules AVICs.
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Ferdous, Zannatul, Hanjoong Jo, and Robert M. Nerem. "Differential Osteogenic Marker Expression by Human Vascular and Valvular Cells in Tissue-Engineered Collagen Constructs." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19424.
Full textAbstract:
Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most patients. However, in spite of the high prevalence, the causes and mechanisms of these diseases are still not clearly understood. Due to the similarities in diseased tissue pathology, atherosclerosis and aortic stenosis have been suggested to be continuum of the same disease [1] and mainly have been investigated for atherosclerosis. However, the prevalence of both diseases is not concurrent in most patients. Likewise, valvular interstitial cells (VICs) were thought to behave in a similar manner as smooth muscle cells (SMCs), but some recent studies suggest differences between the two cell types [2]. Therefore, unique mechanisms might be involved in how VICs and SMCs respond to an osteogenic environment.