Parathyroid-hormone-related Protein Induces Expression of Receptor Activator of NF-κB Ligand in Human Periodontal Ligament Cells <i>via</i> a cAMP/Protein Kinase A-independent Pathway

Fukushima, Hidefumi; Jimi, Eijiro; Kajiya, Hiroshi; Motokawa, Wataru; Okabe, Koji

doi:10.1177/154405910508400407

Cited by 50 publications

(36 citation statements)

References 34 publications

(39 reference statements)

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“…PTHLH stimulates osteoclastogenesis by inducing tartrate-resistant acidic phosphatase in PDL cells, while increasing the receptor activator of the NF-κB ligand and decreasing osteoprotegerin levels (Fukushima et al 2005). PTHLH represses BSP, osteocalcin, and the mineralization in PDL cells and, potentially, in cementoblasts Ouyang et al 2000a,b).…”

Section: Other Peptide Hormonesmentioning

confidence: 99%

Use of microarrays to find novel regulators of periodontal ligament fibroblast differentiation

Lallier

Spencer

2006

Cell Tissue Res

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Periodontal regeneration requires the coordinated movement and differentiation of several cell types in order to re-establish the cementum, periodontal ligament (PDL), and alveolar bone. Cells in culture are often used as model systems for mature tissues, although they may represent expanded progenitor cell populations. Comparison of transcript expression between fresh PDL tissue and PDL cell isolates by MicroArray analysis has revealed numerous molecular differences. Several transcripts (including alkaline phosphatase, bone sialoprotein, periostin, and fibromodulin) are expressed at higher levels in fresh PDL than in cultured PDL cells. In contrast, PDL cells in culture selectively express a variety of growth factors. Several of these growth factors alter PDL fibroblast behavior. Two members of the transforming growth factor beta family of growth factors, namely, bone morphogenic protein-7 (BMP7) and growth differentiation factor-5 (GDF5), reduce cell proliferation and Stro-1 expression (a bone marrow stromal stem cell marker), whereas only BMP7 induces alkaline phosphatase activity. In contrast, fibroblast growth factor-5 induces enhanced cell proliferation and Stro-1 expression, while repressing alkaline phosphatase activity. The stimulation of PDL cells to differentiate (either by BMP7 or GDF5) inhibits cell motility. Thus, PDL cells in culture are regulated by several factors that differentially stimulate a mineralized (cementoblast-like) fate, a non-mineralized fate (mature fibroblasts), or the propagation of a more naive phenotype (potential progenitors).

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Section: Other Peptide Hormonesmentioning

confidence: 99%

Use of microarrays to find novel regulators of periodontal ligament fibroblast differentiation

Lallier

Spencer

2006

Cell Tissue Res

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“…The infl ammatory mediators, such as interleukin (IL)-1 and prostaglandin E 2 (PGE 2 ), induce RANKL expression leading ultimately to alveolar bone loss [3,4] . Studies have demonstrated the expression of RANKL in periodontal tissue and periodontal ligament cells [5][6][7] .…”

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confidence: 99%

Influence of Baicalin on the Expression of Receptor Activator of Nuclear Factor-κB Ligand in Cultured Human Periodontal Ligament Cells

Wang¹,

Wu²,

Wan³

et al. 2006

Pharmacology

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Background: Baicalin is a flavonoid purified from the medicinal plant Scutellaria baicalensis Georgi. It has been reported that baicalin exhibits antibacterial, anti-inflammatory and analgesic effects and can inhibit nuclear factor-ĸB activation. Periodontal disease is a chronic infective disease of the periodontium caused by bacteria present in dental plaque inducing alveolar bone resorption until teeth are lost. Human periodontal ligament (HPDL) is the connective tissue between alveolar bone and tooth. Receptor activator of nuclear factor-ĸB ligand (RANKL), a member of the tumor necrosis factor (TNF) ligand family, plays an important role in osteoclastogenesis from osteoclast precursors to mature osteoclasts. In this study we investigate the effects of baicalin on RANKL protein production and messenger RNA (mRNA) expression induced by IL-1β in cultured HPDL cells. Methods: To induce RANKL expression, IL-1β was added to serum-free medium HPDL cells and incubated. Various concentrations of baicalin (0, 0.001, 0.01 and 0.1 µg/ml) were added to the medium and the cells were treated for 0, 12, 24, 48 and 72 h, respectively. RANKL in the cells was detected using immunocytochemistry. The mRNA of RANKL, osteoprotegerin (OPG) and cyclooxygenase-2 (COX-2) were measured by semiquantitative reverse transcription-polymerase chain reaction. Results: The expression of RANKL at mRNA and protein levels in HPDL cells was stimulated by IL-1β. Baicalin suppressed IL-1β-induced RANKL and COX-2 production at a concentration of 0.01 µg/ml. The most prominent effect was observed with 48 h of baicalin treatment. The inhibition of baicalin on the rhIL-1β-stimulated OPG expression was first apparent at 24 h after the start of treatment, however it did not reach significant differences. Conclusions: The data suggest that baicalin may inhibit RANKL mRNA expression via the suppression of COX-2 expression induced by IL-1β. In addition to its antibacterial and anti-inflammatory properties, baicalin was shown to be effective in periodontitis and alveolar bone resorption.

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“…31 Moreover, coculture of human PDLCs and mouse spleen cells also induced mature osteoclasts. 32 In our study, the conditioned media from the intervening human PDLCs were used to coculture OBs and pre-OCs derived from the rat and successfully produce mature OCs. It further strengthened the previously reported crosstalk between proteins derived from humans and those derived from rodents.…”

Section: Discussionmentioning

confidence: 99%

Compression and hypoxia play independent roles while having combinative effects in the osteoclastogenesis induced by periodontal ligament cells

Yang

et al. 2015

The Angle Orthodontist

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Objective: To investigate the isolated and combined effects of compression and hypoxia on the osteoclastogenesis induced by periodontal ligament cells (PDLCs). Materials and Methods: A periodontal ligament tissue model (PDLtm) was established by 3-D culturing human PDLCs on a thin sheet of poly lactic-co-glycolic acid scaffold. The PDLtm was treated with hypoxia and/or compression for 6, 24, or 72 hours. After that, a real-time polymerase chain reaction was used for gene expression analysis. The conditioned media were used for the coculture of osteoblast and osteoclast (OC) precursors; tartrate-resistant acid phosphatase staining was done to examine OC formation. Results: Either compression or hypoxia alone significantly up-regulated the gene expression of pro-osteoclastogenic cytokines in the PDLtm and enhanced osteoclastogenesis in the cocultures, and the combination of the two had significantly stronger effects than either stimulation alone. In addition, comparing the two stimulants, we found that the osteoclastogenic property of the PDLCs peaked earlier (at 6 hours) in the compression group than in the hypoxia group (at 24 hours). Conclusions: Both compressive force and hypoxia may take part in initiating osteoclastogenesis in orthodontic tooth movement and may have combinatory effects, which could update our concepts of the mechanisms involved in the initiation of bone resorption on the pressure side of the tooth in question. (Angle Orthod. 2016;86:66-73.)

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Parathyroid-hormone-related Protein Induces Expression of Receptor Activator of NF-κB Ligand in Human Periodontal Ligament Cells via a cAMP/Protein Kinase A-independent Pathway

Cited by 50 publications

References 34 publications

Use of microarrays to find novel regulators of periodontal ligament fibroblast differentiation

Use of microarrays to find novel regulators of periodontal ligament fibroblast differentiation

Influence of Baicalin on the Expression of Receptor Activator of Nuclear Factor-κB Ligand in Cultured Human Periodontal Ligament Cells

Compression and hypoxia play independent roles while having combinative effects in the osteoclastogenesis induced by periodontal ligament cells

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