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Estrogen Regulates Expression of Osteoprotegerin and RANKL in Human Periodontal Ligament Cells Through Estrogen Receptor Beta
Author(s) -
Liang Li,
Yu Jifeng,
Wang Yan,
Ding Yin
Publication year - 2008
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2008.070437
Subject(s) - rankl , osteoprotegerin , periodontal fiber , estrogen receptor beta , estrogen receptor , chemistry , medicine , estrogen , small interfering rna , estrogen receptor alpha , endocrinology , receptor , activator (genetics) , microbiology and biotechnology , biology , rna , dentistry , biochemistry , cancer , breast cancer , gene
Background: The function of periodontal ligament (PDL) cells may be affected by estrogen. PDL cells synthesize the receptor activator of nuclear factor‐kappa B ligand (RANKL) and its decoy receptor, namely, osteoprotegerin (OPG), which directly controls osteoclastogenesis. The primary aim of this study was to investigate how estrogen affects the expression of OPG and RANKL in human PDL (hPDL) cells. Methods: We used a short interfering RNA technique to inhibit estrogen receptor beta (ERβ) expression in hPDL cells; the cells were cultured with a saturating concentration of 17β‐estradiol (10 −7 M) for 48 hours. Changes in the expression of OPG and RANKL were determined by reverse transcription‐polymerase chain reaction and supported by Western blot analysis. Results: Estradiol caused an increase in OPG expression and decreased RANKL expression in hPDL cells. However, it had no effect on the expression of OPG and RANKL in hPDL–siERβ (the short interfering RNA to block ER β) cells. Conclusion: Estrogen may play an important role in exerting antiresorptive effects on alveolar bone, at least in part, by increasing the expression level of OPG versus that of RANKL via ERβ in hPDL cells.