PKCα suppresses osteoblastic differentiation

Nakura, Akio; Higuchi, Chikahisa; Yoshida, Kiyoshi; Yoshikawa, Hideki

doi:10.1016/j.bone.2010.09.238

Cited by 36 publications

(33 citation statements)

References 34 publications

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“…These results suggest that PKCa and PKCd inactivation possibly lead to a synergistic increase in Pi-induced VSMC calcification through induction of osteogenic signaling. PKC activation has been reported to suppress extracellular matrix mineralization and osteoblastic differentiation in preosteoblastic MC3T3-E1 and myoblast C2C12 cell lines [21,22], and knockdown of PKC was found to stimulate expression of osteoblast-specific marker genes [21]. Together, these results support the negative effects of PKC activity on both VSMC calcification and osteoblast mineralization.…”

Section: Pkc Inactivation Upregulates Osteogenic Signaling During Piisupporting

confidence: 56%

Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling

Lee

Kim

Jeong

2014

Biochemical and Biophysical Research Communications

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Section: Pkc Inactivation Upregulates Osteogenic Signaling During Piisupporting

confidence: 56%

Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling

Lee

Kim

Jeong

2014

Biochemical and Biophysical Research Communications

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“…However, the function of PKCα in osteoblast differentiation is controversial. PKCα is necessary for basic fibroblast growth factor-induced bone formation (Tang et al, 2004), whereas in MC3T3-E1 cells, overexpression of PKCα decreases ALP activity and attenuates osteoblastic differentiation (Nakura et al, 2011). In this study, we showed that both equol and E 2 upregulated the expression of PKCα, suggesting that the effect of equol on osteoblast proliferation, ALP activity, and osteocalcin content may be mediated by PKCα-related signaling.…”

Section: Discussionsupporting

confidence: 53%

Equol promotes rat osteoblast proliferation and differentiation through activating estrogen receptor

Wang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Phytoestrogens have been suggested as alternative treatment for postmenopausal osteoporosis. Equol, a metabolite of daidzein, has been shown to inhibit bone loss in ovariectomized mice and rats. However, whether or not equol influences the formation of bone has not yet been investigated. Therefore, we investigated the effect of equol on the proliferation and differentiation of rat primary osteoblasts and explored the involved mechanisms. Different equol concentrations significantly promoted the proliferation of osteoblasts after 48-and 72-h incubations. The alkaline phosphatase (ALP) activity also increased significantly in all of the equol and 17β-estradiol (E 2 ) groups, except for the lowest (0.01 µM) equol group. Equol also significantly elevated the osteocalcin levels. The effects of equol on osteoblast proliferation, ALP activity, and osteocalcin levels were blocked by the estrogen receptor (ER) antagonist ICI182780. After a 24-h incubation, the expression of protein kinase C alpha (PKCα) in osteoblasts was significantly increased by equol. In conclusion, our study demonstrated that equol could promote the proliferation and differentiation of rat osteoblasts through activating the ER-PKCα-related signaling pathway, suggesting that equol could promote bone formation. These results suggest that equol could be a potential alternative agent for the management of postmenopausal osteoporosis.

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“…Exposure to mechanical strain rapidly activates PKCα in osteoblast-like cells (29), and PKC signaling has been implicated in the regulation of various mechanically responsive genes, including the osteoblast differentiation marker osteocalcin (30–32). A role for PKCα in regulating osteoblastic cell differentiation has been suggested previously (33). Furthermore, pharmacological activation of PKC signaling rescues defective proliferation of marrow-derived osteoblastic cells in a mouse model in Type I Gaucher disease (34).…”

Section: Introductionmentioning

confidence: 61%

Protein Kinase Cα (PKCα) Regulates Bone Architecture and Osteoblast Activity

Galea

Meakin

Williams

et al. 2014

Journal of Biological Chemistry

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Background: Roles of the multifunctional kinase PKCα in bone are unknown.Results: Female Prkca−/− mice form bone in their medullary cavities associated with higher osteoblastic differentiation. Bone and spleen changes in Prkca−/− mice resemble features of Gaucher disease.Conclusion: PKCα regulates osteoblast differentiation and bone architecture.Significance: PKCα-targeting therapies may benefit low bone mass conditions, including Gaucher disease and osteoporosis.

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PKCα suppresses osteoblastic differentiation

Cited by 36 publications

References 34 publications

Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling

Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling

Equol promotes rat osteoblast proliferation and differentiation through activating estrogen receptor

Protein Kinase Cα (PKCα) Regulates Bone Architecture and Osteoblast Activity

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