Role of the SDF-1/CXCR4 signaling pathway in cartilage and subchondral bone in temporomandibular joint osteoarthritis induced by overloaded functional orthopedics in rats
Role of the SDF-1/CXCR4 signaling pathway in cartilage and subchondral bone in temporomandibular joint osteoarthritis induced by overloaded functional orthopedics in rats
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软骨和软骨下骨中SDF-1/CXCR4信号通路在超负荷功能骨科诱发大鼠颞下颌关节骨关节炎中的作用
DOI：
10.1186/s13018-020-01860-x
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发表时间：
2020-05
影响因子：
2.6
通讯作者：
Xiao Yuan
中科院分区：
文献类型：
--
作者：
Jing Yang;Yazhen Li;Ying Liu;Qiang Zhang;Qi Zhang;Junbo Chen;Xiao Yan;Xiao Yuan
摘要：目的：（i）使用大鼠下颌前移装置研究基质细胞衍生因子/CXC受体4（SDF-1/CXCR 4）信号通路在超负荷功能矫形器（OFO）诱导的颞下颌关节骨关节炎（TMJ OA）中的作用;（ii）为有效治疗骨性II类错牙合和避免TMJ OA提供细胞和分子基础。方法：6周龄雄性SD大鼠随机分为对照组+生理盐水（NS）组、EXP + SDF-1拮抗剂ADM 3100组、EXP + NS组和对照组+ADM 3100组。分别于术后2、4、8周采用苏木精-伊红（H&E）、免疫荧光双染（IDS）、番红-O染色、免疫组化（IHC）、实时荧光定量聚合酶链反应（PCR）和显微CT等方法观察4组关节软骨和软骨下骨的变化。结果：OFO导致SDF-1、CXCR 4和基质金属蛋白酶（MMP）13表达增加，II型胶原表达减少。EXP + NS组4周时软骨肥厚层厚度减少，2周时软骨下骨出现损伤。使用ADM 3100抑制SDF-1信号可以减轻MMP 13的表达、软骨损伤和成骨细胞分化。IDS显示SDF-1和OSX在软骨下骨的表达区域重叠。结论：超负荷的功能矫形术（OFO）诱发了颞下颌关节骨性关节炎。OFO引起的TMJOA软骨下骨破坏先于软骨破坏。SDF-1/CXCR 4可能在OFO引起的TMJOA中诱导成骨分化并引起软骨降解。
Abstract.Objectives.To (i) use a mandibular advancement appliance in rats to investigate the role of the stromal cell-derived factor/CXC receptor 4 (SDF-1/CXCR4) signaling pathway in temporomandibular joint osteoarthritis (TMJ OA) induced by overloaded functional orthopedics (OFO) and (ii) provide a cellular and molecular basis for efficacious treatment of skeletal class-II malocclusion and avoidance of TMJ OA..Method.Male Sprague-Dawley rats (6weeks) were divided randomly into control + normal saline (NS), EXP + ADM3100 (SDF-1 antagonist), EXP + NS, and control + ADM3100 groups. Changes in articular cartilage and subchondral bone after TMJ OA in these four groups were observed by hematoxylin and eosin (H&E), immunofluorescence double staining (IDS), Safranin-O staining, immunohistochemical (IHC) staining, real-time polymerase chain reaction, and micro-computed tomography at 2, 4, and 8 weeks..Results.OFO led to increased expression of SDF-1, CXCR4, and matrix metalloproteinase (MMP) 13 and decreased expression of collagen II. The thickness of the hypertrophic cartilage layer was reduced at 4 weeks in the EXP + NS group, and damage to subchondral bone was observed at 2weeks. Using ADM3100 to inhibit SDF-1 signaling could attenuate expression of MMP13, cartilage damage, and osteoblast differentiation. IDS showed that the areas of expression of SDF-1 and OSX in subchondral bone overlapped..Conclusions.Overloaded functional orthopedics (OFO) induced TMJ OA. The destruction of subchondral bone in TMJ OA caused by OFO occurred before damage to cartilage. SDF-1/CXCR4 may induce the osteogenic differentiation and cause cartilage degradation in TMJ OA caused by OFO.
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影响因子：
5.3
作者：
通讯作者：
--
DOI：
10.1016/j.biocel.2010.03.020
发表时间：
2010-07
影响因子：
4
作者：
Hosogane, Naobumi;Huang, Zhiping;Rawlins, Bernard A.;Liu, Xia;Boachie-Adjei, Oheneba;Boskey, Adele L.;Zhu, Wei
通讯作者：
Zhu, Wei
影响因子：
7
作者：
Liu, Y. -D.;Liao, L. -F.;Zhang, H. -Y.;Lu, L.;Jiao, K.;Zhang, M.;Zhang, J.;He, J. -J.;Wu, Y. -P.;Chen, D.;Wang, M. -Q.
通讯作者：
Wang, M. -Q.
影响因子：
3.7
作者：
Funck-Brentano T;Lin H;Hay E;Ah Kioon MD;Schiltz C;Hannouche D;Nizard R;Lioté F;Orcel P;de Vernejoul MC;Cohen-Solal ME
通讯作者：
Cohen-Solal ME
影响因子：
7.6
作者：
Sobue T;Yeh WC;Chhibber A;Utreja A;Diaz-Doran V;Adams D;Kalajzic Z;Chen J;Wadhwa S
通讯作者：
Wadhwa S