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首页> 外文期刊>APMIS: Acta Pathologica, Microbiologica et Immunologica Scandinavica >Influence of lipopolysaccharide and interleukin-6 on RANKL and OPG expression and release in human periodontal ligament cells.
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Influence of lipopolysaccharide and interleukin-6 on RANKL and OPG expression and release in human periodontal ligament cells.

机译:脂多糖和白介素6对人牙周膜细胞中RANKL和OPG表达和释放的影响。

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摘要

Recent research into periodontal disease pathology focuses on the role of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) in periodontal bone destruction processes. RANKL regulates the differentiation of osteoclast by binding to its specific receptor RANK, while OPG inhibits the differentiation of osteoclasts by binding RANKL and therefore preventing RANKL to bind RANK. The aim of the present study was to investigate the influence of Porphyromonas gingivalis lipopolysaccharide (LPS) and interleukin-6 (IL-6) on RANKL and OPG expression and release in periodontal ligament (PDL) cells. Human PDL cells were stimulated for 48 h with purified P. gingivalis LPS and IL-6. OPG and sRANKL release were assessed by using enzyme-linked immunosorbent assay technique. OPG and RANKL expression was quantitatively measured by using the real-time PCR technique. Whereas P. gingivalis LPS induced sRANKL release, expression was only slightly increased, IL-6 did not show an effect on RANKL expression or release. In conclusion the data demonstrate that stimulation of PDL cells with P. gingivalis LPS leads to an increased release of sRANKL, rather than increased RANKL expression. Through this action, P. gingivalis LPS may exert its biological effect on osteoclast formation and bone resorption.
机译:对牙周疾病病理学的最新研究集中于核因子-κB配体(RANKL)和骨保护素(OPG)的受体激活剂在牙周骨破坏过程中的作用。 RANKL通过与破骨细胞的特异性受体RANK结合来调节破骨细胞的分化,而OPG通过与RANKL结合并因此阻止RANKL与RANK结合来抑制破骨细胞的分化。本研究的目的是研究牙龈卟啉单胞菌脂多糖(LPS)和白介素6(IL-6)对RANKL和OPG在牙周膜(PDL)细胞中表达和释放的影响。用纯化的牙龈卟啉单胞菌LPS和IL-6刺激人PDL细胞48小时。通过使用酶联免疫吸附测定技术评估OPG和sRANKL释放。通过使用实时PCR技术定量测量OPG和RANKL表达。牙龈卟啉单胞菌LPS诱导sRANKL释放,表达仅略有增加,IL-6对RANKL表达或释放没有影响。总之,数据表明用牙龈卟啉单胞菌LPS刺激PDL细胞会导致sRANKL的释放增加,而不是RANKL表达增加。通过该作用,牙龈卟啉单胞菌LPS可对破骨细胞形成和骨吸收发挥其生物学作用。

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