RANKL expression is mediated by p38 MAPK in rat periodontal ligament cells.
10.5051/jkape.2004.34.3.489
- Author:
Chong Cheol KIM
1
;
Young Joon KIM
;
Hyun Ju CHUNG
;
Ok Su KIM
Author Information
1. Department of Periodontology, College of Dentistry and Dental science research institute, Chonnam National University, Korea. youngjun@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
RANKL;
OPG;
p38 MAPK;
periodontal ligament cell;
RT-PCR
- MeSH:
Animals;
Gene Expression;
Humans;
Immunoassay;
MAP Kinase Kinase 4;
Osteoclasts;
p38 Mitogen-Activated Protein Kinases*;
Periodontal Ligament*;
Rats*
- From:The Journal of the Korean Academy of Periodontology
2004;34(3):489-498
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Recent studies have demonstrated that human periodontal ligament cells express receptor activation of nuclear factor kappaB 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-1beta(1 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-1beta 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 NH2-terminal kinase) inhibitor (PD98059) did not regulate mRANKL and mOPG. These results suggested that p38 MAPK play a significant role in RANKL gene expression.
