期刊文献+

肿瘤坏死因子样弱凋亡诱导因子在关节松动假体周围界膜中的表达及临床意义 被引量:7

Expressions and clinical significance of TWEAK in patients with aseptic loosening of prostheses
下载PDF
导出
摘要 目的关节置换术后假体松动一直是关节外科的难题。文中通过探讨肿瘤坏死因子样弱凋亡诱导因子(tumor necrosis factor like weak inducer of apoptosis,TWEAK)在松动假体周围界膜中的表达及其临床意义,进一步了解假体松动的发生机制。方法收集7例髋关节翻修的界膜组织标本为界膜组,同时收集7例因股骨颈骨折行关节置换的髋关节滑膜组织标本为骨折滑膜组,7例因骨性关节炎行关节置换的髋关节滑膜组织标本为关节炎滑膜组。通过形态学观察并采用逆转录PCR(reverse transcription-PCR,RT-PCR)和Western blot检测TWEAK mRNA及TWEAK蛋白在标本中的表达。结果界膜组HE染色可见细胞增生明显并伴有局灶性大量炎性细胞浸润,免疫组化染色见大量TWEAK染色阳性细胞。RT-PCR检测TWEAK mRNA的表达:骨折滑膜组为0.216±0.016,关节炎滑膜组为0.318±0.021,界膜组为0.437±0.008;Western blot检测TWEAK蛋白的表达:骨折滑膜组为0.298±0.014,关节炎滑膜组为0.537±0.033,界膜组为0.715±0.062;TWEAK mRNA和TWEAK蛋白表达,组间两两比较差异均有统计学意义(P<0.05)。结论 TWEAK可能是炎性骨溶解的启动因素之一,进一步探索TWEAK在骨溶解中的作用机制,对临床防治人工关节无菌性松动具有重要意义。 Objective Prosthesis loosening is a problem of joint surgery. We studied the expressions and clinical significance of TWEAK in patients with aseptic loosening of prostheses,and tried to make clear the mechanism of prosthesis loosening. Methods Periprosthetic interface membranes( 7 aseptic loosening of prostheses) were obtained as experimental group and synovial tissues were obtained( 7 osteoarthritis patients and 7 fracture subjects) as control groups. Tissue sections were stained for general morphological characterization. TWEAK mRNA expression in tissues were examined by RT-PCR. TWEAK protein expression were examined by Western blot. Results HE staining showed that a large number of inflammatory cells infiltrated in periprosthetic interface membranes. Immunohistochemical staining also showed that the positive cells markedly increased. The expression levels of TWEAK mRNA was 0. 216 ± 0. 016 in the fracture synovial tissues group,0. 318 ± 0. 021 in osteoarthritis synovial tissues group,and 0. 437 ± 0. 008 in periprosthetic interface membranes group; The expression levels of TWEAK protein was 0. 298 ± 0. 014 in the fracture synovial tissues group,0. 537 ± 0. 033 in osteoarthritis synovial tissues group,and 0.715 ± 0. 062 in periprosthetic interface membranes group( P〈0. 05).Conclusion TWEAK may be the trigger of inflammatory osteolysis. It plays an important role in the pathogenesis of aseptic loosening.
出处 《医学研究生学报》 CAS 北大核心 2015年第2期166-169,共4页 Journal of Medical Postgraduates
基金 江苏省临床医学科技专项基金(BL2012002)
关键词 肿瘤坏死因子样弱凋亡诱导因子 骨溶解 炎性因子 界膜 Tumor necrosis factor like weak inducer of apoptosis Osteolysis Inflammatory factors Periprosthetic interface membranes
  • 相关文献

参考文献17

  • 1Goodman SB. Wear particles, periprosthetic osteolysis and the immune system[ J]. Biomaterials, 2007, 28 (34): 5044-5048.
  • 2Mao X, Pan X, Peng X, et al. Inhibition of titanium particle-in- duced inflammation by the proteasome inhibitor bortezomib in murine macrophage-like RAW 264.7 cells [ J ]. Inflammation, 2012, 35(4) : 1411-1418.
  • 3朱亮亮,赵建宁.人工关节无菌性松动的分子机制及药物干预[J].医学研究生学报,2009,22(3):320-323. 被引量:14
  • 4Gallo J, Goodman SB, Konttinen YT, et al. Particle disease: bi- ologic mechanisms of periprosthetic osteolysis in total hip arthro- plasty[J]. Innate Immunity, 2013, 19(2) : 213-224.
  • 5. Purdue PE, Koulouvaris P, Potter HG, et al. The cellular and molecular biology of periprosthetic osteolysis [ J 1. Clin Orthop Relat Res, 2007, 454 : 251-261.
  • 6Blanco-Colio LM, Martin-Ventura JL, Munoz-Garcia B, et al. TWEAK and Fn14. new players in the pathogenesis of athero- sclerosis [ J]. Front Biosci, 2007, 12 : 3648-3655.
  • 7Desplat-J6go S, Feuillet L, Creidy R, et al. TWEAK is ex- pressed at the cell surface of roonocytes during multiple sclerosis [J]. J Leukoc Biol, 2009, 85(1) : 132-135.
  • 8Winkles JA. The TWEAK-Fnl4 cytokine-receptor axis: discover- y, biology and therapeutic targeting [ J ] Nat Rev Drug Discov, 2008, 7(5) : 411-425.
  • 9Smith MD, Barg E, Weedon H, et al. Microarchitecture and protective mechanisms in synovial tissue from clinically and ar- throscopically normal knee joints [ J ]. Ann Rheum Dis, 2003, 62(4) : 303-307.
  • 10孙国静,杨书丰,郭亭,赵建宁.不同浓度钛合金微粒对成骨细胞信号通路中转录表达因子RUNX2影响[J].医学研究生学报,2013,26(3):251-254. 被引量:10

二级参考文献60

  • 1王扬天,王坚,马驰原.核因子-κB与糖尿病的关系[J].医学研究生学报,2007,20(3):310-314. 被引量:15
  • 2Greenfield M, Bechtold J. What other biologic and mechanical factors might contribute to osteolysis? [ J] Am Acad Ortho Surg, 2007,16( 1 ) :56-62.
  • 3Avbersek-Luznik I, Rus I, Marc J, et al. Increased bone resorption in HD patients: is it caused by elevated RANKL synthesis? [ J] Nephrol Dial Transplant ,2005,20(3) :566-570.
  • 4Vitovski S, Jennifer SP, Sayers J, et al. Investigating the interaction between osteoprotegerin and receptor activator of NF-κB or tumor necrosis factor-related apoptosis-inducing ligand[ J]. Biol Chem,2007,282 ( 43 ) : 31601-31609.
  • 5Yamashita T, Yao ZQ, Li F, et al. NF-κB p50 and p52 regulate receptor activator of NF-κB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1 [J]. Biol Chem,2007,282 (25) : 18245- 18253.
  • 6Clohisy JC, Hirayama T, Frazier E, et al. NF-κB signaling blockade abolishes implant particle-induced osteoclastogenesis [J]. Orthop Res, 2004,22( 1 ) :13-20.
  • 7Clohisy JC, Frazier E, Hirayama T, et al. RANKL is an essential cytokine mediator of polymethylmethacrylate particleinducedoste oclastogenesis[ J]. Orthop Res,2003,21 (2) :202-212.
  • 8Yang SY, Chen W, Stashenko P. Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation[ J]. J Cell Science ,2007,120( 1 ) :3362-3371.
  • 9Sobacchi C, Frattini A, Guerrini MM, et al. Osteoclast-poor osteopetrosis due to mutations in the gene encoding RANKL [ J ]. Nat Geuet ,2007,39 ( 3 ) :960-962.
  • 10Mandelin J, Liljestrom M, Kroon M, et al. Imbalance of RANKL/RANK/OPG system in interface tissue in loosening of total hip replacement [ J ]. Bone Joint Surg Br, 2003,85 (B) : 1196-1201.

共引文献22

同被引文献21

引证文献7

二级引证文献24

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部