Erk pathways negatively regulate matrix mineralization

Kono, Shingo; Oshima, Yasushi; Hoshi, Kazuto; Bonewald, Lynda F.; Oda, Hiromi; Nakamura, Kozo; Kawaguchi, Hiroshi; Tanaka, Sakae

doi:10.1016/j.bone.2006.07.024

Cited by 65 publications

(56 citation statements)

References 28 publications

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“…Altogether, these results suggest that both MAPK and PI-3K pathways could mediate vanadate and insulin anti-mineralogenic effects. We propose that regulation of VSa13 cell differentiation/mineralization is exerted through the PI-3K/ Ras/Erk pathway (a combination of MAPK and PI-3K pathways), a finding that is in agreement with recent results obtained for mouse MC3T3-E1 cells [17]. We further propose, based on overall available data as well as results reported in this study, that a similar mechanism is responsible for transducing vanadate effects (Fig.…”

Section: Putative Pi-3k/ras/erk Pathway Mediates Vanadate Impairment supporting

confidence: 93%

Vanadate proliferative and anti‐mineralogenic effects are mediated by MAPK and PI‐3K/Ras/Erk pathways in a fish chondrocyte cell line

et al. 2008

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We recently reported proliferative and anti-mineralogenic effects of vanadate on fish chondrocytes and here we investigate the signalling pathways associated with these effects. Our data show that vanadate stimulates chondrocyte proliferation through the MAPK pathway, using signalling mechanisms similar to those used by IGF-1, while it inhibits chondrocyte differentiation/mineralization through a putative PI-3K/Ras/ Erk signalling, a pathway shared with insulin. Our data also suggest that vanadate impairs ECM mineralization not only by interfering with regulatory pathways but also by inhibiting enzymatic activity of ALP. Finally, this work provides additional evidence for the conservation, throughout evolution, of mechanisms regulating chondrocyte proliferation and differentiation.

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Section: Putative Pi-3k/ras/erk Pathway Mediates Vanadate Impairment supporting

confidence: 93%

Vanadate proliferative and anti‐mineralogenic effects are mediated by MAPK and PI‐3K/Ras/Erk pathways in a fish chondrocyte cell line

et al. 2008

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“…FAK is involved in the regulation of cell growth and survival through activation mainly to different pathways, PI3K/PKD1/ Akt/PKB and Grb2/SOS/Ras/Raf-1/MEK/ERK. We have focused on the Ras/ERK pathway because of its known involvement in signal transduction events associated with fibroblast/ osteoblast differentiation (25,26). Therefore, we next sought to study stretch-mediated MAPK activation.…”

Section: Eph Receptors and Ephrin Ligands Are Expressed By Pdlfmentioning

confidence: 99%

Strain-dependent Up-regulation of Ephrin-B2 Protein in Periodontal Ligament Fibroblasts Contributes to Osteogenesis during Tooth Movement

Diercke

Kohl

Lux

et al. 2011

Journal of Biological Chemistry

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Background: Regulation of bone remodeling during orthodontic tooth movement. Results: Tensile stress induces ephrin-B2 expression in PDL fibroblasts, and ephrin-B2-EphB4 interactions induce osteoblastogenesis in osteoblasts of the alveolar bone. Conclusion: Ephrin-B2-EphB4 signaling between PDLF and osteoblasts of the alveolar bone might contribute to bone remodeling during orthodontic tooth movement. Significance: Understanding the regulation of bone remodeling during orthodontic tooth movement is a prerequisite for pharmacological interventions.

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“…Based on published results, we suggest that vanadate inhibitory effect on VSa13 ECM mineralization could be associated with either direct interference of vanadium into key processes such as alkaline phosphatase activity, or indirect interference of vanadium into insulin-associated pathways. Recently, it was shown that the ECM mineralization of MC3T3-E1 cells is inhibited by platelet-derived growth factor through ERK activation (Kono et al 2007). This result is, on one hand, contradictory to a previous observation where ECM mineralization of MC3T3-E1 cells was stimulated by vanadium through ERK activation (Cortizo et al 2006), but, on the other hand, in total agreement with the inhibition of VSa13 ECM mineralization by vanadate, possibly through ERK activation.…”

Section: Inhibition Of Ecm Mineralization By Vanadatementioning

confidence: 99%

Impairment of mineralization by metavanadate and decavanadate solutions in a fish bone-derived cell line

et al. 2007

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Vanadium, a trace metal known to accumulate in bone and to mimic insulin, has been shown to regulate mammalian bone formation using in vitro and in vivo systems. In the present work, short-and long-term effects of metavanadate (containing monomeric, dimeric, tetrameric and pentameric vanadate species) and decavanadate (containing decameric vanadate species) solutions on the mineralization of a fish bone-derived cell line (VSa13) were studied and compared to that of insulin. After 2 h of incubation with vanadate (10 μM in monomeric vanadate), metavanadate exhibited higher accumulation rates than decavanadate (6.85±0.40 versus 3.95± 0.10 μg V/g of protein, respectively) in fish VSa13 cells and was also shown to be less toxic when applied for short periods. In longer treatments with both metavanadate and decavanadate solutions, similar effects were promoted: stimulation of cell proliferation and strong impairment (75%) of extracellular matrix (ECM) mineralization. The effect of both vanadate solutions (5 μM in monomeric vanadate), on ECM mineralization was increased in the presence of insulin (10 nM). It is concluded that chronic treatment with both vanadate solutions stimulated fish VSa13 cells proliferation and prevented ECM mineralization. Newly developed VSa13 fish cells appeared to be appropriate in the characterization of vanadate effects on vertebrate bone formation, representing a good alternative to mammalian systems.

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Erk pathways negatively regulate matrix mineralization

Cited by 65 publications

References 28 publications

Vanadate proliferative and anti‐mineralogenic effects are mediated by MAPK and PI‐3K/Ras/Erk pathways in a fish chondrocyte cell line

Vanadate proliferative and anti‐mineralogenic effects are mediated by MAPK and PI‐3K/Ras/Erk pathways in a fish chondrocyte cell line

Strain-dependent Up-regulation of Ephrin-B2 Protein in Periodontal Ligament Fibroblasts Contributes to Osteogenesis during Tooth Movement

Impairment of mineralization by metavanadate and decavanadate solutions in a fish bone-derived cell line

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