Effect of F-spondin on cementoblastic differentiation of human periodontal ligament cells

Kitagawa, Masae; Kudo, Yasusei; Iizuka, Shinji; Ogawa, Ikuko; Abiko, Yoshimitsu; Miyauchi, Mutsumi; Takata, Takashi

doi:10.1016/j.bbrc.2006.08.142

Cited by 59 publications

(73 citation statements)

References 21 publications

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“…In the present study, we used a PDLC line immortalized by hTERT transfection (Kitagawa et al 2006), which retains the features of their original primary cells (i.e., PDLCs). Thus, this immortalized cell line is a helpful tool for studying the biology and mechanisms of PDLCs.…”

Section: Discussionmentioning

confidence: 99%

“…Immortalized human dental periodontal ligament cells transfected with the human telomerase catalytic component (hTERT) were kindly provided by Professor Takashi Takata (Hiroshima University, Japan; Kitagawa et al 2006). Cells were cultured at 37 °C in Minimal Essential Medium α (α-MEM) supplemented with 10% fetal bovine serum (FBS), 100 U/mL penicillin, and 100 µg/mL streptomycin in a humidified atmosphere of 5% CO 2 .…”

Section: Cell Culturementioning

confidence: 99%

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PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

et al. 2014

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Inflammatory responses and osteoclast differentiation play pivotal roles in the pathogenesis of osteolytic bone diseases such as periodontitis. Although overexpression or inhibition of peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (PIN1) offers a possible therapeutic strategy for chronic inflammatory diseases, the role of PIN1 in periodontal disease is unclear. The aim of the present study was to evaluate PIN1 expression in periodontitis patients as well as the effects of PIN1 inhibition by juglone or PIN1 small-interfering RNA (siRNA) and of PIN1 overexpression using a recombinant adenovirus encoding PIN1 (Ad-PIN1) on the inflammatory response and osteoclastic differentiation in lipopolysaccharide (LPS)-and nicotine-stimulated human periodontal ligament cells (PDLCs). PIN1 was up-regulated in chronically inflamed PDLCs from periodontitis patients and in LPS-and nicotine-exposed PDLCs. Inhibition of PIN1 by juglone or knockdown of PIN1 gene expression by siRNA markedly attenuated LPS-and nicotine-stimulated prostaglandin E 2 (PGE 2 ) and nitric oxide (NO) production, as well as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, whereas PIN1 overexpression by Ad-PIN1 increased it. LPS-and nicotine-induced nuclear factor (NF)-κB activation was blocked by juglone and PIN1 siRNA but increased by Ad-PIN1. Conditioned medium prepared from LPS-and nicotinetreated PDLCs increased the number of tartrate-resistant acid phosphatase-stained osteoclasts and osteoclast-specific gene expression. These responses were blocked by PIN1 inhibition and silencing but stimulated by Ad-PIN1. Furthermore, juglone and PIN1 siRNA inhibited LPS-and nicotine-induced osteoclastogenic cytokine expression in PDLCs. This study is the first to demonstrate that PIN1 inhibition exhibits anti-inflammatory effects and blocks osteoclastic differentiation in LPS-and nicotine-treated PDLCs. PIN1 inhibition may be a therapeutic strategy for inflammatory osteolysis in periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

et al. 2014

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“…A cell line of cementoblasts has recently been established in mice and humans, and differentiation markers such as CP-23, CEMP1, and F-spondin have been identified (1,9,20).…”

Section: Cell Growth Ratementioning

confidence: 99%

Response to light compressive force in human cementoblasts in vitro

et al. 2016

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The objective of this study is to investigate the responses of human cementoblasts to light compressive force in vitro. A human cementoblast cell line (HCEM) was loaded for 12 h by mounting coverslips (0.25 gf/cm 2 ). The coverslips were removed and the cells were cultured for up to 21 days. Cells without glass loading were used as controls. Cell growth, morphological changes, and the mRNA expression of RUNX2, ALP, WNT5A and SPON1 were investigated. No significant differences were observed in cell numbers between the compressed group and control group. Morphology of the compressed cells was slightly flattened on day 0; however, no indications of cell death were detected. Expression of differentiation markers including RUNX2, ALP and WNT5A was significantly lower in the compressed group (0.7, 0.75 and 0.75-fold respectively, P < 0.05) than in the control group on day 7. The expression levels of SPON1, a differentiation marker of cementoblasts, were higher on days 7 and 14 than on day 0, but were lower in the compressed group than in the control group (P < 0.01). These results suggest that light compressive force does not affect cell growth and morphology, but restrains higher expression of cementogenic differentiation markers in human cementoblasts in vitro.

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“…Immortalized hPDLCs 21) transfected with human telomerase catalytic component (hTERT), were kindly provided by Professor Takashi Takata (Hiroshima University, Japan). The cells were cultured in -modified Eagle medium (-MEM) supplemented with 10% fetal bovine serum (FBS), 100 U/mL penicillin, and 100 g/mL streptomycin in a humidified atmosphere of 5% CO2 at 37 o C. -MEM, FBS, and penicillin/streptomycin were purchased from Gibco BRL Co. (Grand Island, NY, USA).…”

Section: Cell Culturementioning

confidence: 99%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and PGE2 and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and PGE2 release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

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Effect of F-spondin on cementoblastic differentiation of human periodontal ligament cells

Cited by 59 publications

References 21 publications

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

<b>Response to light compressive force in human cementoblasts </b><i><b>in </b></i><i><b>vitro </b></i>

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

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