腰椎间盘退行性改变患者ADAMTS-7表达及其机制研究
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摘要
目的探讨新型金属蛋白酶(ADAMTS-7)在腰椎间盘退行性改变患者中表达情况,并探讨其作用机制。方法2014年3月至2016年2月我院手术切除腰椎间盘突出症患者退变的椎间盘组织40例(依据后外层纤维破裂与否分为破裂组及未破裂组)及同期腰椎骨折患者正常腰椎间盘组织20例(对照组),采用半定量RT-PCR及免疫组织化学技术对不同髓核组织中肿瘤坏死因子(TNF-α)、ADAMTS-7进行定性定量检测。结果 TNF-α表达量随腰椎间盘退变程度加重而增加,ADAMTS-7蛋白在对照组腰椎间盘髓核组织呈现弱阳性表达,在未破裂组及破裂组椎间盘髓核组织中分别呈阳性表达及强阳性表达;3组ADAMTS-7蛋白表达量、mRNA表达量及TNF-αmRNA表达量由高到低排序为破裂组>未破裂组>对照组(P<0.05)。结论 ADAMTS-7及TNF-α在腰椎间盘退行性改变患者髓核组织中存在高表达现象,并且退变程度越重其表达量越多,而作用机制可能与7 ADAMTS-7及TNF-α在腰椎间盘退行性病变中表达呈正反馈通路加速其病程进展有关。
Objective To investigate the expression of new type metalloproteinase( ADAMTS-7) in patients with degenerative lumbar disc and explore its mechanism.Methods The degenerative lumbar disc tissue samples from 40 patients with lumbar disc herniation undergoing the surgical resection of the degenerative disc tissue in our hospital from March 2014 to February 2016 were collected.The samples were divided into the rupture group and the non-rupture group based on whether the posterior outer fiber ruptured or not.At the same time,normal lumber disc tissue samples from 20 patients with lumbar vertebrae fractures were also collected as the control group.Qualitative and quantitative detection of tumor necrosis factor α( TNF-α) and ADAMTS-7 were performed by using semiquantitative RT-PCR and immunohistochemistry.Results The expression levels of TNF-α was increased with the degree of degeneration of lumbar intervertebral disc.ADAMTS-7 protein was shown weakly positive expression in the nucleus pulposus of the lumbar intervertebral disc in the control group while it was positive and strongly positive expression in the nucleus pulposus of the rupture group and the non-rupture group.The expression levels of ADAMTS-7 protein,mRNA and TNF-α in the three groups ranged from high to low: the rupture group > the non-rupture group > the control group( P < 0. 05). Conclusion There are high expressions of ADAMTS-7 and TNF-α in the nucleus pulposus of patients with degenerative changes in lumbar intervertebral disc.The more serious degeneration is,the higher expression level is.The mechanism may be related to the expressions of ADAMTS-7 and TNF-α as the positive feedback pathways,which can accelerate the disease progression of the degenerative lesions in lumbar intervertebral disc.
Objective To investigate the expression of new type metalloproteinase( ADAMTS-7) in patients with degenerative lumbar disc and explore its mechanism.Methods The degenerative lumbar disc tissue samples from 40 patients with lumbar disc herniation undergoing the surgical resection of the degenerative disc tissue in our hospital from March 2014 to February 2016 were collected.The samples were divided into the rupture group and the non-rupture group based on whether the posterior outer fiber ruptured or not.At the same time,normal lumber disc tissue samples from 20 patients with lumbar vertebrae fractures were also collected as the control group.Qualitative and quantitative detection of tumor necrosis factor α( TNF-α) and ADAMTS-7 were performed by using semiquantitative RT-PCR and immunohistochemistry.Results The expression levels of TNF-α was increased with the degree of degeneration of lumbar intervertebral disc.ADAMTS-7 protein was shown weakly positive expression in the nucleus pulposus of the lumbar intervertebral disc in the control group while it was positive and strongly positive expression in the nucleus pulposus of the rupture group and the non-rupture group.The expression levels of ADAMTS-7 protein,mRNA and TNF-α in the three groups ranged from high to low: the rupture group > the non-rupture group > the control group( P < 0. 05). Conclusion There are high expressions of ADAMTS-7 and TNF-α in the nucleus pulposus of patients with degenerative changes in lumbar intervertebral disc.The more serious degeneration is,the higher expression level is.The mechanism may be related to the expressions of ADAMTS-7 and TNF-α as the positive feedback pathways,which can accelerate the disease progression of the degenerative lesions in lumbar intervertebral disc.
引文
[1]殷相姣,宫赫,王丽珍,等.椎间盘退行性变的影响因素及其相关形态结构变化的研究进展[J].生物医学工程与临床,2016,26(1):112-117.
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[10]史东,董富强,董金波,等.ADAMTS-4、ADAMTS-5在骨关节炎患者滑膜中的表达及意义[J].现代预防医学,2015,42(6):1061-1064.
[11]Stanton H,Melrose J,Little CB,et al.Proteoglycan degradation by the ADAMTS family of proteinases[J].Biochimicaet Biophysica Acta(BBA)-Molecular Basis of Disease,2011,1812(12):1616-1629.
[12]殷浩,贺学军,易惠军,等.CT表现与临床定位体征不相符的腰椎间盘突出症MSCT重建图像分析[J].实用医院临床杂志,2014,11(1):86-88.
[13]Lai Y,Bai X,Zhao Y,et al.ADAMTS-7 forms a positive feedback loop with TNF-αin the pathogenesis of osteoarthritis[J].Annals of the Rheumatic Diseases,2014,73(8):1575-84.
[2]张海青,蒋大海.腰椎间盘退行性病变诊断中CT与MRI的应用价值[J].中国现代医生,2016,54(19):101-103.
[3]褚相乐,马景旭,邱雪玲,等.DTI在腰椎间盘退行性改变中的应用初探[J].放射学实践,2016,31(1):81-85.
[4]SS Wang,WZhang,YQ Zhang,等.IL-17 A enhances ADAMTS-7 expression through regulation of TNF-αin human nucleus pulposus cells[J].Journal of Molecular Histology,2015,46(6):475.
[5]董视师,李景峰,周逸驰,等.腰椎间盘退变:组织工程修复及生物力学评价[J].中国组织工程研究,2015,19(37):6024-6030.
[6]Lin EA,Liu CJ.The emerging roles of ADAMTS-7 and ADAMTS-12matrix metalloproteinases[J].Open Access Rheumatology:Research and Reviews,2009,1(1):121-131.
[7]王利,王宪,孔炜.新型金属蛋白酶ADAMTS家族的研究进展[J].生理科学进展,2008,39(1):49-52.
[8]魏凡华,张玉颖,于修平.基质金属蛋白酶ADAMTS的研究进展[J].中国细胞生物学学报,2014,26(8):1186-1192.
[9]李俊杰,梁舒涵,彭奇,等.椎间盘退行性变的信号转导机制研究进展[J].山东医药,2015,29(48):90-92.
[10]史东,董富强,董金波,等.ADAMTS-4、ADAMTS-5在骨关节炎患者滑膜中的表达及意义[J].现代预防医学,2015,42(6):1061-1064.
[11]Stanton H,Melrose J,Little CB,et al.Proteoglycan degradation by the ADAMTS family of proteinases[J].Biochimicaet Biophysica Acta(BBA)-Molecular Basis of Disease,2011,1812(12):1616-1629.
[12]殷浩,贺学军,易惠军,等.CT表现与临床定位体征不相符的腰椎间盘突出症MSCT重建图像分析[J].实用医院临床杂志,2014,11(1):86-88.
[13]Lai Y,Bai X,Zhao Y,et al.ADAMTS-7 forms a positive feedback loop with TNF-αin the pathogenesis of osteoarthritis[J].Annals of the Rheumatic Diseases,2014,73(8):1575-84.