Calmodulin-dependent kinase II regulates osteoblast differentiation through regulation of Osterix

Choi, You Hee; Choi, Jun-Ha; Oh, Jae-Wook; Lee, Kwang-Youl

doi:10.1016/j.bbrc.2013.02.005

Cited by 33 publications

(29 citation statements)

References 27 publications

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“…However, any increase in calcium levels leads to the activation of calcineurin, which induces its dephosphorylation and translocation to the nucleus, in which NFAT acts as a resorption activator. However, Lee, 2013;Koga et al, 2005;Ueki et al, 2008). Thus, we analyzed the Nfatc1 mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

Frizzled 6 disruption suppresses osteoblast differentiation induced by nanotopography through the canonical Wnt signaling pathway

Abuna

Oliveira

Adolpho

et al. 2020

Journal Cellular Physiology

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This study aimed to investigate if wingless‐related integration site (Wnt) signaling participates in the high osteogenic potential of titanium with nanotopography (Ti‐Nano). We showed that among the several components of the Wnt signaling pathway, Frizzled 6 (Fzd6) was the transcript most intensely modulated by nanotopography compared with the untreated Ti surface (Ti‐Machined). Then, we investigated whether and how Fzd6 participates in the regulation of osteoblast differentiation caused by nanotopography. The Fzd6 silencing with CRISPR–Cas9 transfection in MC3T3‐E1 cells induced a more pronounced inhibition of osteoblast differentiation of cells cultured on nanotopography than those cultured on Ti‐Machined. The analysis of the expression of calcium‐calmodulin‐dependent protein kinase II and β‐catenin demonstrated that Fzd6 disruption inhibited the osteoblast differentiation induced by Ti‐Nano by preventing the activation of Wnt/β‐catenin but not that of Wnt/Ca2+ signaling, which is usually triggered by the receptor Fzd6. These findings elucidate the biological function of Fzd6 as a receptor that triggers Wnt/β‐catenin signaling and the cellular mechanisms modulated by nanotopography during osteoblast differentiation.

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Section: Discussionmentioning

confidence: 99%

Frizzled 6 disruption suppresses osteoblast differentiation induced by nanotopography through the canonical Wnt signaling pathway

Abuna

Oliveira

Adolpho

et al. 2020

Journal Cellular Physiology

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“…[27][28][29][30] Nakashima et al 27 showed that inactivation of the Osx gene in mice resulted in little to no bone formation. Osterix (SP7, Osx) is an osteoblast-specific zinc-finger transcription factor that is critical to the development and production of bone tissue.…”

Section: Discussionmentioning

confidence: 99%

“…calmodulin-dependent kinase II, 30 Wnt/β-catenin, 31,32 and Runx2. 33 All of these molecules are involved in the development of osteoblasts and maintenance of mature bone tissue although Runx2 is also associated with the development of cells having chondrogenic potential.…”

Section: Discussionmentioning

confidence: 99%

A Method for the Immunohistochemical Identification and Localization of Osterix in Periosteum-Wrapped Constructs for Tissue Engineering of Bone

McClellan

Jacquet

et al. 2017

J Histochem Cytochem.

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A novel immunohistochemistry (IHC) approach has been developed to label and localize osterix, a bone-specific transcription factor, within formalin-fixed, paraffin-embedded, tissue-engineered constructs uniquely containing synthetic polymers and human periosteal tissue. Generally, such specimens consisting in part of polymeric materials and mineral are particularly difficult for IHC identification of proteins. Samples here were fabricated from human periosteum, electrospun poly-l-lactic acid (PLLA) nanofibers, and polycaprolactone/poly-l-lactic acid (PCL/PLLA, 75/25) scaffolds and harvested following 10 weeks of implantation in athymic mice. Heat-induced and protease-induced epitope retrieval methods from selected existing protocols were examined to identify osterix. All such protease-induced techniques were unsuccessful. Heat-induced retrieval gave positive results for osterix immunohistochemical staining in sodium citrate/EDTA/Tween 20 with high heat (120C) and pressure (~30 psi) for 10 min, but the heat and pressure levels resulted in tissue damage and section delamination from slides that limited protocol effectiveness. Heat-induced epitope retrieval led to other osterix-positive staining results achieved with minimal impact on structural integrity of the tissue and polymers in sodium citrate/EDTA/Tween 20 buffer at 60C and normal pressure (14.5 psi) for 72 hr. The latter approach identified osterix-positive cells by IHC within periosteal tissue, layers of electrospun PLLA nanofibers, and underlying PCL/PLLA scaffolds of the tissue-engineered constructs.

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“…Furthermore, studies have demonstrated that peptidyl‐prolyl isomerase 1 (Pin1) and several kinases such as protein kinase A (PKA), glycogen synthase kinase 3‐alpha (GSK3‐α) and calmodulin‐dependent kinase II (CaMKII) could modulate the function of Osx at post‐translational level through phosphorylation, regulation of protein stabilization and transcriptional activity (Choi et al . , Li et al . , He et al .…”

Section: Regulatory Mechanisms Of Osx Expressionmentioning

confidence: 99%

Site‐specific function and regulation of Osterix in tooth root formation

Sui

et al. 2016

Int Endodontic J

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Congenital diseases of tooth roots, in terms of developmental abnormalities of short and thin root phenotypes, can lead to loss of teeth. A more complete understanding of the genetic molecular pathways and biological processes controlling tooth root formation is required. Recent studies have revealed that Osterix (Osx), a key mesenchymal transcriptional factor participating in both the processes of osteogenesis and odontogenesis, plays a vital role underlying the mechanisms of developmental differences between root and crown. During tooth development, Osx expression has been identified from late embryonic to postnatal stages when the tooth root develops, particularly in odontoblasts and cementoblasts to promote their differentiation and mineralization. Furthermore, the site-specific function of Osx in tooth root formation has been confirmed, because odontoblastic Osx-conditional knockout mice demonstrate primarily short and thin root phenotypes with no apparent abnormalities in the crown (Journal of Bone and Mineral Research 30, 2014 and 742, Journal of Dental Research 94, 2015 and 430). These findings suggest that Osx functions to promote odontoblast and cementoblast differentiation and root elongation only in root, but not in crown formation. Mechanistic research shows regulatory networks of Osx expression, which can be controlled through manipulating the epithelial BMP signalling, mesenchymal Runx2 expression and cellular phosphorylation levels, indicating feasible routes of promoting Osx expression postnatally (Journal of Cellular Biochemistry 114, 2013 and 975). In this regard, a promising approach might be available to regenerate the congenitally diseased root and that regenerative therapy would be the best choice for patients with developmental tooth diseases.

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Calmodulin-dependent kinase II regulates osteoblast differentiation through regulation of Osterix

Cited by 33 publications

References 27 publications

Frizzled 6 disruption suppresses osteoblast differentiation induced by nanotopography through the canonical Wnt signaling pathway

Frizzled 6 disruption suppresses osteoblast differentiation induced by nanotopography through the canonical Wnt signaling pathway

A Method for the Immunohistochemical Identification and Localization of Osterix in Periosteum-Wrapped Constructs for Tissue Engineering of Bone

Site‐specific function and regulation of Osterix in tooth root formation

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