Effect of hypoxia on the expression of CCAAT/enhancer-binding protein β and receptor activator of nuclear factor kappa-B ligand in periodontal ligament cells

Access this Article

Search this Article

Author(s)

    • Ito Hisanori
    • Department of Pediatric Dentistry, Nihon University School of Dentistry
    • Kifune Takashi
    • Department of Pediatric Dentistry, Nihon University School of Dentistry
    • Ishiyama Misa
    • Department of Pediatric Dentistry, Nihon University School of Dentistry
    • Iwasa Satoko
    • Department of Pediatric Dentistry, Nihon University School of Dentistry
    • Takei Hiroki
    • Department of Pediatric Dentistry, Nihon University School of Dentistry
    • Shirakawa Tetsuo
    • Department of Pediatric Dentistry, Nihon University School of Dentistry|Division of Oral and Craniomaxillofacial Research, Dental Research Center, Nihon University School of Dentistry

Abstract

<p>Hypoxia after traumatic injuries to a tooth is one of the causes of subsequent root resorption. Inflammatory cytokines produced under hypoxic conditions are associated with root resorption, but the mechanism has not been fully understood. In this study, the role of hypoxia-inducible factor-1 (HIF-1) signaling in the regulation of CCAAT (cytosine-cytosine-adenosine-adenosine-thymidine)/enhancer-binding protein-β (C/EBPβ) and the receptor activator of nuclear factor kappa-B ligand (RANKL) expressions in immortalized human periodontal ligament (PDL) cells was investigated. PDL cells cultured under a hypoxic condition showed an increase in the expression of C/EBPβ and RANKL messenger RNAs (mRNAs), whereas the expression of osteoprotegerin and HIF-1α mRNAs was unaffected. Hypoxia had no effects on the secretion of interleukin (IL)-1β, IL-6, IL-8, IL-17A, tumor necrosis factor-alpha, macrophage migration inhibitory factor, monocyte chemoattractant protein-1, and macrophage colony-stimulating factor in the culture media. Treatment of the cells with dimethyloxaloylglycine, a competitive HIF prolyl hydroxylase inhibitor, significantly increased the expression of C/EBPβ and RANKL mRNAs. This suggested that the hypoxia-induced elevation of C/EBPβ and RANKL mRNAs was dependent on the HIF-1 activity. PDL cells transfected with a specific small interfering RNA designed to target the C/EBPβ gene showed a significant suppression of the RANKL mRNA. These findings indicated that C/EBPβ may play an important role in tooth root resorption via RANKL activation in hypoxia-exposed PDL cells.</p>

Journal

  • Journal of Oral Science

    Journal of Oral Science 60(4), 544-551, 2018

    Nihon University School of Dentistry

Codes

Page Top