Promotion of Bone Regeneration by CCN2 Incorporated into Gelatin Hydrogel

Kikuchi, Takeshi; Kubota, Satoshi; Asaumi, Koji; Kawaki, Harumi; Nishida, Takashi; Kawata, Kazumi; Mitani, Shigeru; Tabata, Yasuhiko; Ozaki, Toshifumi; Takigawa, Masaharu

doi:10.1089/tea.2007.0167

Cited by 11 publications

(12 citation statements)

References 41 publications

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“…Authors: The microvibration regimen was determined based on existing literatures and our preliminary studies. The optimal parameters of vibration in our study are different from those in vitro and in vivo studies (Rubin et al, 2002;Rubin et al, 2004;Garman et al, 2007;Lau et al, 2010;Patel et al, 2009, text references;Rubin et al, 2001;Maddalozzo et al;2008, de Oliveira et al, 2010. The disparity may due to the various factors, including different devices to produce vibration, different culturing environment and cell types for in vitro study, different subjects for in vivo study, and different conditions between in vivo and in vitro study.…”

Section: Wwwecmjournalorg Y Zhou Et Al Osteogenic Differentiation mentioning

confidence: 61%

“…Authors: It has been recently been shown by many in vivo studies that LMHF vibration and other kinds of mechanical stimuli exhibit favourable infl uence on bone homeostasis (Rubin et al, 2002;Rubin et al, 2004;Ward et al, 2004;Garman et al, 2007;Rubin et al, 2007, text references;Rubin et al, 2001;Maddalozzo et al, 2008;de Oliveira et al, 2010, additional references). Although the anabolic role of LMHF vibration on bone is achieved by different magnitudes and frequencies of vibration produced with different devices, the time for vibration imposed on these objects is temporal and intermittent.…”

Section: Discussion With Reviewersmentioning

confidence: 99%

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Osteogenic differentiation of bone marrow-derived mesenchymal stromal cells on bone-derived scaffolds: effect of microvibration and role of ERK1/2 activation

Zhou

Guan²,

Zhu³

et al. 2011

eCM

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Although in vivo studies have shown that low-magnitude, high-frequency (LMHF) vibration (LM: < 1 ×g; HF: 20-90 Hz) exhibits anabolic effects on skeletal homeostasis, the underlying cellular/molecular regulation involved in bone adaptation to LMHF vibration is little known.In this report, we tested the effects of microvibration (magnitude: 0.3 ×g, frequency: 40 Hz, amplitude: ±50 μm, 30 min/12 h) on proliferation and osteodifferentiation of bone marrow-derived mesenchymal stromal cells (BMSCs) seeded on human bone-derived scaffolds. The scaffolds were prepared by partial demineralisation and deproteinisation. BMSCs were allowed to attach to the scaffolds for 3 days. Morphological study showed that spindle-shaped BMSCs almost completely covered the surface of bone-derived scaffold and these cells expressed higher ALP activity than those cultured on plates. After microvibration treatment, BMSC proliferation was decreased on day 7 and 10; however, numbers of genes and proteins expressed during osteogenesis, including Cbfa1, ALP, collagen I and osteocalcin were greatly increased. ERK1/2 activation was involved in microvibration-induced BMSC osteogenesis. Taken together, this study suggests that bone-derived scaffolds have good biocompatibility and show osteoinductive properties. By increasing the osteogenic lineage commitment of BMSCs and enhancing osteogenic gene expressions, microvibration promotes BMSC differentiation and increase bone formation of BMSCs seeded on bone-derived scaffolds. Moreover, ERK1/2 pathway plays an important role in microvibrationinduced osteogenesis in BMSC cellular scaffolds.Keywords: Bone-derived scaffold, bone marrow-derived mesenchymal stromal cells, microvibration, osteogenesis, ERK1/2. *Address for correspondence: Haiyang Yu West China Hospital of Stomatology Sichuan University Chengdu, 610041, P.R. China Telephone/FAX Number: 86-028-85502869 E-mail: yhyang6812@scu.edu.cn IntroductionCurrent consensus for bone tissue engineering includes three essential elements, i.e., biomaterial scaffold, osteogenic cell lineage and bone inducing factors (e.g., mechanical stimulus, Ashammakhi and Ferretti, 2003; Khan et al., 2005;Mistry and Mikos, 2005). Scaffold materials should provide the support for cell attachment and have osteoinductive property (Langer and Vacanti, 1993;Ashammakhi and Ferretti, 2003). Due to the limited supply and donor-site morbidity of autogenous bone grafts, different physical structures and insuffi cient osteoinductive ability of synthetic materials (Ashammakhi and Ferretti, 2003;Silber et al., 2003), scaffolds derived from different individuals (allografts) and species (xenografts) provide a promising resource and approach to address the signifi cant drawbacks of existing scaffolds, because these scaffolds have similar structures to autogenous bone (Salkeld et al., 2001;Simion et al., 2004). Additionally, with the proper chemical and physical process on these bone materials, including demineralisation and deproteinisation (Tadjoedin et al., 2003;Xu et al., 2003...

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Section: Wwwecmjournalorg Y Zhou Et Al Osteogenic Differentiation mentioning

confidence: 61%

Section: Discussion With Reviewersmentioning

confidence: 99%

Osteogenic differentiation of bone marrow-derived mesenchymal stromal cells on bone-derived scaffolds: effect of microvibration and role of ERK1/2 activation

Zhou

Guan²,

Zhu³

et al. 2011

eCM

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“…One of the classical family members, CCN2, is known to be a key factor that promotes harmonized development and regeneration of mesenchymal tissues (Kikuchi et al 2008;Ono et al 2008;Kubota and Takigawa 2011). Nevertheless, the distinct profibrotic function of this same molecule has been widely recognized as well, which function is firmly supported by scientific evidence presented by a number of investigators.…”

Section: Introductionmentioning

confidence: 97%

Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family

Kader

Kubota

Janune

et al. 2012

J. Cell Commun. Signal.

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CCN family proteins 2 and 3 (CCN2 and CCN3) belong to the CCN family of proteins, all having a high level of structural similarity. It is widely known that CCN2 is a profibrotic molecule that mediates the development of fibrotic disorders in many different tissues and organs. In contrast, CCN3 has been recently suggested to act as an anti-fibrotic factor in several tissues. This CCN3 action was shown earlier to be exerted by the repression of the CCN2 gene expression in kidney tissue, whereas different findings were obtained for liver cells. Thus, the molecular action of CCN3 yielding its anti-fibrotic effect is still controversial. Here, using a general model of fibrosis, we evaluated the effect of CCN3 overexpression on the gene expression of all of the CCN family members, as well as on that of fibrotic marker genes. As a result, repression of CCN2 gene expression was modest, while type I collagen and α-smooth muscle actin gene expression was prominently repressed. Interestingly, not only CCN2, but also CCN4 gene expression showed a decrease upon CCN3 overexpression. These findings indicate that fibrotic gene induction is under the control of a complex molecular network conducted by CCN family members functioning together.

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“…4). Of note, CCN2 in the gelatin hydrogel enables gradual release of CCN2 in vivo up to 14 days (Kikuchi et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis

El-Seoudi

Kader

Nishida

et al. 2017

J. Cell Commun. Signal.

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Fibroblast growth factor 1 (FGF-1) is a classical member of the FGF family and is produced by chondrocytes cultured from osteoarthritic patients. Also, this growth factor was shown to bind to CCN family protein 2 (CCN2), which regenerates damaged articular cartilage and counteracts osteoarthritis (OA) in an animal model. However, the pathophysiological role of FGF-1 in cartilage has not been well investigated. In this study, we evaluated the effects of FGF-1 in vitro and its production in vivo by use of an OA model. Treatment of human chondrocytic cells with FGF-1 resulted in marked repression of genes for cartilaginous extracellular matrix components, whereas it strongly induced matrix metalloproteinase 13 (MMP-13), representing its catabolic effects on cartilage. Interestingly, expression of the CCN2 gene was dramatically repressed by FGF-1, which repression eventually caused the reduced production of CCN2 protein from the chondrocytic cells. The results of a reporter gene assay revealed that this repression could be ascribed, at least in part, to transcriptional regulation. In contrast, the gene expression of FGF-1 was enhanced by exogenous FGF-1, indicating a positive feedback system in these cells. Of note, induction of FGF-1 was observed in the articular cartilage of a rat OA model. These results collectively indicate a pathological role of FGF-1 in OA development, which includes an insufficient cartilage regeneration response caused by CCN2 down regulation.

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Promotion of Bone Regeneration by CCN2 Incorporated into Gelatin Hydrogel

Cited by 11 publications

References 41 publications

Osteogenic differentiation of bone marrow-derived mesenchymal stromal cells on bone-derived scaffolds: effect of microvibration and role of ERK1/2 activation

Osteogenic differentiation of bone marrow-derived mesenchymal stromal cells on bone-derived scaffolds: effect of microvibration and role of ERK1/2 activation

Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family

Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis

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