Effects of core binding factor α1 or bone morphogenic protein‐2 overexpression on osteoblast/cementoblast‐related gene expressions in NIH3T3 mouse cells and dental follicle cells

Pan, Keqing; Yan, Shihao; Ge, Shaohua; Li, S; Zhao, Yijiao; Yang, Pishan

doi:10.1111/j.1365-2184.2009.00599.x

Cited by 12 publications

(15 citation statements)

References 53 publications

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“…(2) Elevated mRNA expressions of several osteoblast marker genes (SP7, OCN, and BSP) in LV-Runx2 cells. This was in consistent with its role in promoting the osteodifferentiation of many osteoblastic and nonosteoblastic cells, such as bone marrow stromal cells (BMSC), MC3T3-E1 pre-osteoblasts, NIH3T3 fibroblasts, dental follicle cells, myoblasts, and adipose (Xiao et al, 1999;Byers et al, 2004;Gersbach et al, 2004;Zhang et al, 2006;Pan et al, 2009). Secondly, CMT loading activated ERK1/2 pathway and significantly elevated mRNA expressions of SP7, OCN, and BSP, while inhibiting ERK1/2 by U0126 dramatically attenuated these augmentations.…”

Section: The Effect Of Cmt On Osteodifferentiation Of Hpdlfssupporting

confidence: 67%

Phosphorylation of Runx2, induced by cyclic mechanical tension via ERK1/2 pathway, contributes to osteodifferentiation of human periodontal ligament fibroblasts

Ren

Wei

et al. 2015

Journal Cellular Physiology

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Occlusal force is an important stimulus for maintaining periodontal homeostasis. This is attributed to the quality of human periodontal ligament fibroblasts (hPDLFs) that could transfer occlusal force into biological signals modulating osteoblst differentiation. However, few studies investigated the mechanism of occlusal force-induced osteodifferentiation of hPDLFs. In our study, we used the cyclic mechanical tension (CMT) at 10% elongation with 0.5 Hz to mimic occlusal force, and explored its effects on osteogenesis of hPDLFs. Firstly, elevated expressions of several osteoblast marker genes (Runx2, ATF4, SP7, OCN, and BSP), as well as activated ERK1/2 pathway were detected during CMT loading for 1, 3, 6, 12, 18, and 24 h. To gain further insight into how CMT contributed to those effects, we focused on the classic ERK1/2-Runx2 pathway by inhibiting ERK1/2 and overexpressing Runx2. Our results reflected that Runx2 overexpression alone could induce osteodifferentiation of hPDLFs. Meanwhile, CMT loading could intensify while combined ERK1/2 blockage could weaken this process. Furthermore, we found that CMT promoted Runx2 transcription and phosphorylation via ERK1/2; protein level of phospho-Runx2 (p-Runx2), rather than Runx2, was in parallel with mRNA expressions of SP7, OCN, and BSP. Taken together, our study proved that p-Runx2, elevated by CMT via ERK1/2 pathway, is the predominate factor in promoting osteoblast differentiation of hPDLFs.

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Section: The Effect Of Cmt On Osteodifferentiation Of Hpdlfssupporting

confidence: 67%

Phosphorylation of Runx2, induced by cyclic mechanical tension via ERK1/2 pathway, contributes to osteodifferentiation of human periodontal ligament fibroblasts

Ren

Wei

et al. 2015

Journal Cellular Physiology

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“…Runx‐2 overexpression in the osteoblast‐like cell line UMR‐106 leads to the induction of osteoblast ECM protein expression and mineralized nodule formation (Geoffroy et al, ). In another study, overexpression of Runx‐2 by retroviral infection, induced osteoblast‐related gene expression levels, such as mRNA levels of ALP, Col I, and BSP in murine fibroblast cell line (NIH3T3) cells and in dental follicle cells (DFC) (Pan et al, ). In vitro experiments demonstrate that Runx‐2 transfection induce ALP activity in multipotential mesenchymal cells, C3H10T1/2 and C2C12, indicating an important role for Runx‐2 in the induction of ALP activity (Harada et al, ; Lee et al, ).…”

Section: Discussionmentioning

confidence: 99%

Transgenic Expression of Osteoactivin/gpnmb Enhances Bone Formation In Vivo and Osteoprogenitor Differentiation Ex Vivo

Frara

Abdelmagid

Sondag

et al. 2015

Journal Cellular Physiology

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Initial identification of osteoactivin (OA)/glycoprotein non-melanoma clone B (gpnmb) was demonstrated in an osteopetrotic rat model, where OA expression was increased 3-fold in mutant bones, compared to normal. OA mRNA and protein expression increase during active bone regeneration post-fracture, and primary rat osteoblasts show increased OA expression during differentiation in vitro. To further examine OA/gpnmb as an osteoinductive agent, we characterized the skeletal phenotype of transgenic mouse overexpressing OA/gpnmb under the CMV-promoter (OA-Tg). Western blot analysis showed increased OA/gpnmb in OA-Tg osteoblasts, compared to wild-type (WT). In OA-Tg mouse femurs versus WT littermates, micro-CT analysis showed increased trabecular bone volume and thickness, and cortical bone thickness; histomorphometry showed increased osteoblast numbers, bone formation and mineral apposition rates in OA-Tg mice; and biomechanical testing showed higher peak moment and stiffness. Given that OA/gpnmb is also over-expressed in osteoclasts in OA-Tg mice, we evaluated bone resorption by ELISA and histomorphometry, and observed decreased serum CTX-1 and RANK-L, and decreased osteoclast numbers in OA-Tg, compared to WT mice, indicating decreased bone remodeling in OA-Tg mice. The proliferation rate of OA-Tg osteoblasts in vitro was higher, compared to WT, as was alkaline phosphatase staining and activity, the latter indicating enhanced differentiation of OA-Tg osteoprogenitors. Quantitative RT-PCR analysis showed increased TGF-β1 and TGF-β receptors I and II expression in OA-Tg osteoblasts, compared to WT. Together, these data suggest that OA overexpression has an osteoinductive effect on bone mass in vivo and stimulates osteoprogenitor differentiation ex vivo.

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“…Non‐adherent tissues were removed 24 h later and medium was changed every 3 days. Expressions of mesenchymal marker vimentin and epithelial marker cytokeratin in these cultured cells were determined by immunohistochemical analysis, and DFCs were identified as vimentin‐positive and cytokeratin‐negative cells as described previously (17–20). DFCs at up to three passages were used for further experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Retroviral plasmid pLEGFP‐IRES‐Runx2, encoding full‐length mouse Runx2 cDNA with MASNSL as the N‐terminal sequence, was constructed as described previously (19). Mutant Runx2 without VWRPY motif was generated from plasmid pCMV5‐Cbfa1 (kindly provided by Dr Patricia Ducy, University of Texas M. D. Anderson Cancer Center).…”

Section: Methodsmentioning

confidence: 99%

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Multilineage differentiation of dental follicle cells and the roles of Runx2 over‐expression in enhancing osteoblast/cementoblast‐related gene expression in dental follicle cells

et al. 2010

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Effects of core binding factor α1 or bone morphogenic protein‐2 overexpression on osteoblast/cementoblast‐related gene expressions in NIH3T3 mouse cells and dental follicle cells

Abstract: CBFA1 overexpression up-regulated expression levels of osteoblast/cementoblast-related genes and enhanced in vitro osteogenic differentiation more efficiently than BMP-2 in both NIH3T3 cells and DFCs.

Cited by 12 publications

References 53 publications

Phosphorylation of Runx2, induced by cyclic mechanical tension via ERK1/2 pathway, contributes to osteodifferentiation of human periodontal ligament fibroblasts

Phosphorylation of Runx2, induced by cyclic mechanical tension via ERK1/2 pathway, contributes to osteodifferentiation of human periodontal ligament fibroblasts

Transgenic Expression of Osteoactivin/gpnmb Enhances Bone Formation In Vivo and Osteoprogenitor Differentiation Ex Vivo

Multilineage differentiation of dental follicle cells and the roles of Runx2 over‐expression in enhancing osteoblast/cementoblast‐related gene expression in dental follicle cells

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