仿骨保护素小分子活性多肽的设计及其对破骨活动的影响

doi:10.13701/j.cnki.kqyxyj.2022.05.017

口腔医学研究 ›› 2022, Vol. 38 ›› Issue (5): 477-481.DOI: 10.13701/j.cnki.kqyxyj.2022.05.017

仿骨保护素小分子活性多肽的设计及其对破骨活动的影响

王江玥¹, 吴刚², 田野¹, 白丁^1*

1.四川大学华西口腔医院正畸科国家口腔疾病重点实验室四川成都 610041;
2.荷兰阿姆斯特丹大学和阿姆斯特丹自由大学阿姆斯特丹牙科学术中心口腔种植和修复学系(ACTA) 阿姆斯特丹 999023

收稿日期:2021-10-25 出版日期:2022-05-28 发布日期:2022-05-20
通讯作者: *白丁,E-mail: baiding@scu.edu.cn
作者简介:王江玥(1996~ ),女,河北保定人,博士在读,研究方向:错牙合畸形矫治中成骨破骨活动机制。
基金资助:
国家自然科学基金(编号:81870804) 四川省自然科学基金(编号:2021YJ0014)

Inhibition of Osteoclastogenesis by A Designed Osteoprotegerin-like Peptide

WANG Jiangyue¹, WU Gang², TIAN Ye¹, BAI Ding^1*

1. West China Hospital of Stomatology, State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Sichuan University, Chengdu 610041, China;
2. Department of Oral Implantology and Prosthetic Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije Universiteit, Amsterdam 999023, Netherlands

Received:2021-10-25 Online:2022-05-28 Published:2022-05-20

摘要/Abstract

摘要： 目的: 设计并探究仿骨保护素(osteoprotegerin,OPG)小分子活性多肽是否具有抑制破骨细胞分化作用,及其抑制破骨的可能机制。方法: 以OPG与核因子-κB受体活化因子配体(receptor activator of nuclear factor kappa-B ligand, RANKL)结合位点氨基酸序列为依据设计小分子活性多肽OPGL 1、2、3,以50 μmol/L浓度加入RANKL诱导的破骨细胞前体细胞,通过抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase, TRAP)染色检测破骨细胞数目,实时荧光定量PCR检测破骨表型基因TRAP、CTSK和通路基因NFATC1表达情况,Western blot检测破骨表型蛋白TRAP和C-fos表达情况。结果: 3条小分子活性多肽中,OPGL2有效抑制破骨分化,下调TRAP、CKST、NFATC1基因并抑制TRAP、C-fos蛋白表达。结论: 仿OPG小分子活性多肽OPGL2可以有效抑制破骨向分化,其可能通路为NFATC1。

关键词: 破骨细胞, 活性肽, 骨保护素, 抗酒石酸酸性磷酸酶

Abstract: Objective: To design and investigate the role of peptides mimicking the binding site of osteoprotegerin (OPG) in inhibiting osteoclastogenesis and its possible mechanism. Methods: Fifty micromolar osteoprotegerin-like peptides OPGL 1, 2, and 3 were added to RANKL-induced osteoclast precursor. Tartrate-resistant acid phosphatase (TRAP) osteoclast phenotype staining, quantitative real-time PCR, and Western blot were used to test the ability of peptides. Results: OPGL2 appeared to significantly suppress RANK-induced osteoclastogenesis and led to decreased expression of TRAP, Cathepsin K (CTSK), and NFATC1 gene. OPGL2 also inhibited the expression of osteoclast-related proteins such as TRAP and C-fos. Conclusion: OPGL2 osteoprotegerin-like peptide could inhibit osteoclast differentiation, and its possible pathway was NFATC1.

Key words: osteoclast, peptide, osteoprotegerin, tartrate-resistant acid phosphatase

王江玥, 吴刚, 田野, 白丁. 仿骨保护素小分子活性多肽的设计及其对破骨活动的影响[J]. 口腔医学研究, 2022, 38(5): 477-481.

WANG Jiangyue, WU Gang, TIAN Ye, BAI Ding. Inhibition of Osteoclastogenesis by A Designed Osteoprotegerin-like Peptide[J]. Journal of Oral Science Research, 2022, 38(5): 477-481.

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仿骨保护素小分子活性多肽的设计及其对破骨活动的影响

Inhibition of Osteoclastogenesis by A Designed Osteoprotegerin-like Peptide

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