RANKL expression is mediated by p38 MAPK in rat periodontal ligament cells

백서 치주인대세포의 RANKL 발현에 대한 p38 MAPK의 역할

  • Kim, Chong-Cheol (Dept. of Periodontology, College of Dentistry and Dental science research institute, Chonnam National University) ;
  • Kim, Young-Joon (Dept. of Periodontology, College of Dentistry and Dental science research institute, Chonnam National University) ;
  • Chung, Hyun-Ju (Dept. of Periodontology, College of Dentistry and Dental science research institute, Chonnam National University) ;
  • Kim, Ok-Su (Dept. of Periodontology, College of Dentistry and Dental science research institute, Chonnam National University)
  • 김종철 (전남대학교 치과대학 치주과학교실 및 치의학연구소) ;
  • 김영준 (전남대학교 치과대학 치주과학교실 및 치의학연구소) ;
  • 정현주 (전남대학교 치과대학 치주과학교실 및 치의학연구소) ;
  • 김옥수 (전남대학교 치과대학 치주과학교실 및 치의학연구소)
  • Published : 2004.09.30

Abstract

Recent studies have demonstrated that human periodontal ligament cells express receptor activation of nuclear factor ${\kappa}B$ ligand (RANKL) which enhances the bone resorbing activity of osteoclasts differentiated from hematopoietic preosteoclasts. The purpose of this study is to determine the effects of p38 MAPK and JNK kinase upon regulating RANKL and OPG in response to $IL-1{\beta}$(l ng/ml) in rat periodontal ligament cells. Soluble RANKL was measured by immunoassay. The effects of p38 MAPK on RANKL and OPG expression was determined by RT-PCR. The results were as follows: 1. Periodontal ligament cells which stimulated by $IL-1{\beta}$ increased soluble RANKL synthesis by dose-dependent pattern. 2. p38 MAP kinase inhibitor (SB203580) showed regulation of soluble RANKL expression by dose-dependent manners. 3. p38 MAP kinase inhibitor (SB203580) regulated the expression of RANKL, but it dose regulate the expresseion of OPG. 4. JNK (c-jun $NH_2-terminal$ kinase) inhibitor (PD98059) did not regulate mRANKL and mOPG. These results suggested that p38 MAPK play a significant role in RANKL gene expression.

Keywords

References

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