The Expression And Regulation Of Estrogen Receptor-related Receptor α In Periodontal Ligament Cells

Estrogen deficiency is important in the pathogenesis of postmenopausal osteoporosis. Estrogen plays important roles in the development of bone cells and maintains the bone morphologically. The loss of the bone mass caused by postmenopausal osteoporosis can be reversed by the estrogen replacement therapy. The physiological effects of estrogen are mainly mediated by estrogen receptor (ER)α/βwhich both belong to the nuclear receptor superfamily. Estrogen receptor-related receptorαwere identified by low-stringency screening of cDNA libraries with a probe encompassing the DNA binding domain of human ERα, which is the first-found orphan nuclear receptor. Previous researches have demonstrated the important role of ERRαplaying in the regulation of bone metabolism and the impinging on the estrogen pathway.Periodontal ligament cells (PDLCs) are crucial on maintaining the periodontal ligament morphologically and functionally, and play important roles in the modeling and remodeling of the alveolar bone. Previously, the expression of ERα/βin PDLCs has been described, so did the enhancement of osteogenic effects of PDLCs stimulated by estradial (E2). We wonder whether ERRαare also expressed in PDLCs and intervenes the E2 signals mediated by ERs. Thus,following experiment were designed and carried out:1. We investigated the expression of ERRαin periodontal tissues of SD-rats by immunohistochemistry. The result showed the extensive expression of ERRα in rat periodontal ligament. The in situ study demonstrated the existence of ERRαin rat periodontal tissues.2. By cell culture of human PDLCs (hPDLCs), we investigated the expression of ERRαin the cells. The results of immunocytochemistry and RT-PCR respectly show the expression of ERRαprotain and mRNA in hPDLCs. It proved that ERRαexists in hPDLCs.3. By real-time quantative PCR, we found that in both of the untreated group and the E2-treated group of hPDLCs, the expression of ERRαwas fluctuated similarly during the 20 days in culture. However, the stimulus of E2 inhibited the expression of ERRα, and by the treatment of osteogenic medium, the expression of ERRαsharply increased at the mineral stage of the cells. The results imply that E2 inhibited the expression of ERRαin hPDLCs, and the osteogenic medium promotes the expression of ERRαin the mineral stage of hPDLCs.