Penolazzi Letizia, Magri Eros, Lambertini Elisabetta, Calò Girolamo, Cozzani Mauro, Siciliani Giuseppe, Piva Roberta, Gambari Roberto
ER-GenTech, Department of Biochemistry and Molecular Biology, Molecular Biology Section, University of Ferrara, Ferrara, Italy.
Int J Mol Med. 2006 Nov;18(5):807-11.
In this study, we report the in vivo effects of a decoy oligonucleotide targeting the nuclear factor kappaB (NF-kappaB) on osteoclasts during forced orthodontic tooth movement in rats. Wistar rats were subjected to orthodontic forces, in the absence or presence of treatment with a decoy molecule mimicking a nonsymmetric NF-kappaB binding site (5'-CGC TGG GGA CTT TCC ACG G-3'). TUNEL staining of fragmented DNA revealed that treatment with NF-kappaB decoy but not with scramble double-stranded oligodeoxynucleotides (ODN) induced a high level of osteoclast apoptosis in vivo. Immunohystochemical analysis for death receptor Fas revealed strong positivity only in samples treated with NF-kappaB decoys, demonstrating that osteoclasts are sensitive to death induction via Fas signaling. Induction of apoptosis in osteoclasts could be a strategy for treatment of excessive osteoclast activity in pathologic conditions such as osteoporosis, peri-articular osteolysis, inflammatory arthritis, Paget's syndrome and tumour-associated osteolytic metastases.
在本研究中,我们报告了靶向核因子κB(NF-κB)的诱饵寡核苷酸在大鼠强迫性正畸牙齿移动过程中对破骨细胞的体内作用。将Wistar大鼠施加正畸力,在不存在或存在模拟非对称NF-κB结合位点(5'-CGC TGG GGA CTT TCC ACG G-3')的诱饵分子治疗的情况下。对片段化DNA进行TUNEL染色显示,用NF-κB诱饵而非随机双链寡脱氧核苷酸(ODN)处理可在体内诱导高水平的破骨细胞凋亡。对死亡受体Fas的免疫组织化学分析显示,仅在用NF-κB诱饵处理的样本中呈强阳性,表明破骨细胞对通过Fas信号传导诱导的死亡敏感。诱导破骨细胞凋亡可能是治疗骨质疏松症、关节周围骨质溶解、炎性关节炎、佩吉特氏病和肿瘤相关溶骨性转移等病理状况下破骨细胞过度活跃的一种策略。