論文

査読有り
2017年4月

Ameloblastin and enamelin prevent osteoclast formation by suppressing RANKL expression via MAPK signaling pathway

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Wichida Chaweewannakorn
  • ,
  • Wataru Ariyoshi
  • ,
  • Toshinori Okinaga
  • ,
  • Kazumasa Morikawa
  • ,
  • Katsura Saeki
  • ,
  • Kenshi Maki
  • ,
  • Tatsuji Nishihara

485
3
開始ページ
621
終了ページ
626
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2017.01.181
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Ameloblastin (Ambn) and enamelin (Enam) play a pivotal role in enamel mineralization. Previous studies have demonstrated that these enamel-related gene products also affect bone growth and remodeling; however, the underlying mechanisms have not been elucidated. In the present study, we examined the effects of Ambn and Enam on the receptor activator of nuclear factor kappa-B ligand (RANKL) expression induced with 1,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3) and dexamethasone (DEX) on mouse bone marrow stromal cell line ST2 cells. We then verified the effect of Ambn and Enam on osteoclastogenesis. We found that pretreatment with recombinant human Ambn (rhAmbn) and recombinant human Enam (rhEnam) remarkably suppressed RANKL mRNA and protein expression induced with 1,25(OH)2D3 and DEX. Interestingly, rhAmbn and rhEnam attenuated the phosphorylation of mitogen-activated protein kinases (MAPK), including ERK1/2, JNK, and p38 in ST2 cells stimulated with 1,25(OH)2D3 and DEX. Moreover, pretreatment with specific inhibitors of ERK1/2 and p38, but not JNK, blocked RANKL mRNA and protein expression. Cell co-culture results showed that rhAmbn and rhEnam downregulated mouse bone marrow cell differentiation into osteoclasts induced with 1,25(OH)2D3 and DEX-stimulated ST2 cells. These results suggest that Ambn and Enam may indirectly suppress RANKL-induced osteoclastogenesis via downregulation of p38 and ERK1/2 MAPK signaling pathways in bone marrow stromal cells. (C) 2017 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2017.01.181
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28161637
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000398011300008&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2017.01.181
  • ISSN : 0006-291X
  • eISSN : 1090-2104
  • PubMed ID : 28161637
  • Web of Science ID : WOS:000398011300008

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