广西壮族人群8q24.21区域单核苷酸多态性与腰椎退行性疾病的相关性:800例资料分析
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摘要
背景:基于北欧人群的全基因组关联分析研究发现8q24.21区域的单核苷酸多态性与腰椎间盘突出存在相关性,但由于存在种族差异性,其研究结果在其他人群尚未验证。目的:探讨在广西壮族人群中8q24.21区域单核苷酸多态性与腰椎退行性疾病是否存在相关性。方法:病例组为2015年1月至2016年12月住院治疗的腰椎退行性疾病的壮族患者400例,对照组为年龄匹配的正常壮族成年人400名。试验获得广西医科大学附属第一医院的伦理委员会批准。所有受试者均自愿入组,并签署知情同意书。根据MRI影像学特征,将病例组分为腰椎间盘突出、腰椎滑脱、腰椎管狭窄3个亚组。提取受试者基因组DNA,运用TaqMan探针技术对8q24.21区域rs7816342、rs4130415位点进行PCR荧光分型;并比较各组的等位基因频率、基因型频率分布差异。结果与结论:①rs7816342、rs4130415位点的等位基因频率和基因型频率在病例组和对照组间差异无显著性意义(基因型:rs7816342;P=0.370,rs4130415,P=0.668),但上述2个位点的基因型频率,在腰椎管狭窄组和对照组间差异有显著性意义(基因型:rs7816342,P=0.008;rs4130415,P=0.006);②结果提示8q24.21区域rs7816342、rs4130415位点基因多态性与腰椎管狭窄存在显著相关性。
BACKGROUND: A genome-wide association analysis performed on North European shows that single nucleotide polymorphism(8q24.21) is related to lumbar disc herniation, but the result in the other populations has not been confirmed. OBJECTIVE: To investigate the association between single nucleotide polymorphism(8q24.21) and lumbar degenerative disease in Guangxi Zhuang population. METHODS: Four hundred Zhuang populations with lumbar degenerative disease from January 2015 to December 2016 were selected as case group, and 400 healthy Zhuang adults as control group. The study was approved by the Ethics Committee of the First Affiliated Hospital of Guangxi Medical University. All participants were voluntary to the study and signed the informed consents. The case group was assigned into three subgroups based on MRI performance: lumbar disc herniation, lumbar spondylolisthesis, and lumbar spinal stenosis. The genomic DNA was extracted, and rs7816342 and rs4130415(8q24.21) typing was detected by TaqMan prob. The distribution difference of allele frequency and genotype frequency was compared. RESULTS AND CONCLUSION:(1) The allele frequency and genotype frequency of rs7816342 and rs4130415(8q24.21) showed no significant difference between two groups(rs7816342, P=0.370; rs4130415, P=0.668). The genotype frequency of rs7816342 and rs4130415 was significantly different between lumbar spinal stenosis and control groups(rs7816342, P=0.008; rs4130415, P=0.006).(2) In summary, rs7816342 and rs4130415 polymorphism(8q24.21) is associated with lumbar spinal stenosis.
BACKGROUND: A genome-wide association analysis performed on North European shows that single nucleotide polymorphism(8q24.21) is related to lumbar disc herniation, but the result in the other populations has not been confirmed. OBJECTIVE: To investigate the association between single nucleotide polymorphism(8q24.21) and lumbar degenerative disease in Guangxi Zhuang population. METHODS: Four hundred Zhuang populations with lumbar degenerative disease from January 2015 to December 2016 were selected as case group, and 400 healthy Zhuang adults as control group. The study was approved by the Ethics Committee of the First Affiliated Hospital of Guangxi Medical University. All participants were voluntary to the study and signed the informed consents. The case group was assigned into three subgroups based on MRI performance: lumbar disc herniation, lumbar spondylolisthesis, and lumbar spinal stenosis. The genomic DNA was extracted, and rs7816342 and rs4130415(8q24.21) typing was detected by TaqMan prob. The distribution difference of allele frequency and genotype frequency was compared. RESULTS AND CONCLUSION:(1) The allele frequency and genotype frequency of rs7816342 and rs4130415(8q24.21) showed no significant difference between two groups(rs7816342, P=0.370; rs4130415, P=0.668). The genotype frequency of rs7816342 and rs4130415 was significantly different between lumbar spinal stenosis and control groups(rs7816342, P=0.008; rs4130415, P=0.006).(2) In summary, rs7816342 and rs4130415 polymorphism(8q24.21) is associated with lumbar spinal stenosis.
引文
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[14]Arnbak B,Jensen RK,Manniche C,et al.Identification of subgroups of inflammatory and degenerative MRI findings in the spine and sacroiliac joints:a latent class analysis of 1037 patients with persistent low back pain.Arthritis Res Ther.2016;18(1):237.
[15]Muriuki MG, Havey RM,Voronov LI,et al. Effects of motion segment level, Pfirrmann intervertebral disc degeneration grade and gender on lumbar spine kinematics.J Orthop Res.2016;34(8):1389-1398.
[16]Xiao L,Ni CL,Shi JD,et al.Analysis of Correlation Between Vertebral Endplate Change and Lumbar Disc Degeneration.Medical Science Monitor.2017;23:4932-4938.
[17]Wu B,Meng C,Wang H,et al.Changes of proteoglycan and collagen II of the adjacent intervertebral disc in the cervical instability models. Biomed Pharmacother.2016; 84:754-758.
[18]Grant MP,Epure LM,Bokhari R,et al.Human cartilaginous endplate degeneration is induced by calcium and the extracellular calcium-sensing receptor in the intervertebral disc. Eur Cell Mater.2016;32:137-151.
[19]Xu HG,Zheng Q,Song JX,et al.Intermittent cyclic mechanical tension promotes endplate cartilage degeneration via canonical Wnt signaling pathway and E-cadherin/beta-catenin complex cross-talk. Osteoarthritis Cartilage. 2016;24(1):158-168.
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[21]Garnero P. The Role of Collagen Organization on the Properties of Bone. Calcif Tissue Int. 2015,97(3):229-240.
[22]张学利,宋海峰,朱如森,等.Ⅸ型胶原蛋白A2基因多态性与环境因素在腰椎间盘退变疾病中的作用[J]中华实验外科杂志,2017, 34(7):1232-1235.
[23]Wu HH, Wang ST, Chen WY, et al. Collagen IX gene polymorphisms and lumbar disc degeneration:a systematic review and meta-analysis. J Orthop Surg Res. 2018;13(1):47.
[24]Mio F, Chiba K, Hirose Y, et al. A functional polymorphism in COL11A1, which encodes the alpha 1 chain of type XI collagen, is associated with susceptibility to lumbar disc herniation[J]. Am J Hum Genet.2007;81(6):1271-1277.
[25]Ruel N, Markova DZ,Adams SL,et al.Fibronectin fragments and the cleaving enzyme ADAM-8 in the degenerative human intervertebral disc.Spine(Phila Pa 1976).2014; 39(16):1274-1279.
[26]Urano T,Narusawa K,Shiraki M,et al.Single-nucleotide polymorphism in the hyaluronan and proteoglycan link protein 1(HAPLN1)gene is associated with spinal osteophyte formation and disc degeneration in Japanese women. Eur Spine J.2011;20(4):572-577.
[27]S M H, M K S, G K C, et al. Association of CILP, COL9A2 and MMP3 Gene Polymorphisms with Lumbar Disc Degeneration in an Indian Population.J Mol Neurosci.2018;66(3):378-382.
[28]Li Y, Li K, Han XG, et al. The imbalance between TIMP3 and matrix-degrading enzymes plays an important role in intervertebral disc degeneration. Biochemical and Biophysical Research Communications, 2016, 469(3):507-514.
[29]张博,杨少华,林世洲,等.基质金属蛋白酶1在不同程度退变腰椎间盘髓核与纤维环中的表达及意义[J].中国组织工程研究, 2012,16(13):2346-2349.
[30]Deng B, Ren JZ, Meng XQ, et al. Expression profiles of MMP-1and TIMP-1 in lumbar intervertebral disc degeneration. Genet Mol Res.2015;14(4):19080-19086.
[31]Yuan HY, Tang Y, Lei L, et al.[Synergistic interaction between MMP-3, VDR gene polymorphisms and occupational risk factors on lumbar disc degeneration]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi.2010;28(5):334-338.
[32]Williams FMK, Bansal AT, van Meurs JB, et al. Novel genetic variants associated with lumbar disc degeneration in northern Europeans:a meta-analysis of 4600 subjects. Annals of the Rheumatic Diseases, 2013, 72(7):1141-1148.
[33]Lin WP,Lin JH,Chen XW,et al.Interleukin-10 promoter polymorphisms associated with susceptibility to lumbar disc degeneration in a Chinese cohort.Genet Mol Res.2011;10(3):1719-1727.
[34]Omair A,Lie BA,Reikeras O, et al. An Association Study of Interleukin 18 Receptor Genes(IL18R1 and IL18RAP)in Lumbar Disc Degeneration. Open Orthop J.2012; 6:164-171.
[35]Jiang H, Qin Z,Zong S,et al. Vitamin D receptor gene polymorphisms and lumbar disc degeneration:a systematic review and meta-analysis. Eur Spine J.2017;26(1):267-277.
[36]Zawilla NH, Darweesh H, Mansour N,et al. Matrix metalloproteinase-3, vitamin D receptor gene polymorphisms, and occupational risk factors in lumbar disc degeneration. J Occup Rehabil.2014; 24(2):370-381.
[37]Yuan HY,Tang Y,Liang YX,et al.Matrix metalloproteinase-3 and vitamin d receptor genetic polymorphisms, and their interactions with occupational exposure in lumbar disc degeneration. J Occup Health.2010;52(1):23-30.
[38]Schultz DR,Harrington WJ Jr.. Apoptosis:Programmed cell death at a molecular level. Semin Arthritis Rheum. 2003;32(6):345-369.
[39]Ariga K,Yonenobu K,Nakase T,et al.Mechanical stress-induced apoptosis of endplate chondrocytes in organ-cultured mouse intervertebral discs-An ex vivo study.Spine.2003; 28(14):1528-1533.
[40]Sakai D, Nakamura Y, Nakai T, et al. Exhaustion of nucleus pulposus progenitor cells with ageing and degeneration of the intervertebral disc. Nat Commun.2012;3:1264.
[41]Jiang M, Zhu K, Grenet J, et al.Retinoic acid induces caspase-8transcription via phospho-CREB and increases apoptotic responses to death stimuli in neuroblastoma cells. Biochim Biophys Acta. 2008;1783(6):1055-1067.
[42]Wang X, Luo T, Ruan M, et al. Association of the CCDC26rs4295627 polymorphism with the risk of glioma:Evidence from7,290 cases and 11,630 controls. Mol Clin Oncol.2016;4(5):878-882.
[43]Cao K, Li M, Miao J, et al. CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.Am J Transl Res.2018;10(1):274-282.
[44]Zeng J, Luo Y, Yu M, et al.CCDC26 rs4295627 polymorphisms associated with an increased risk of glioma:A meta-analysis. Adv Clin Exp Med.2017; 26(8):1275-1281.
[45]Peng Wand Jiang A.Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. Biomed Pharmacother.2016;83:712-717.
[46]Wang SL, Hui YZ, Li XM, et al. Silencing of lncRNA CCDC26Restrains the Growth and Migration of Glioma Cells In Vitro and In Vivo via Targeting miR-203.Oncology Res.2018; 26(8):1143-1154.
[47]Izadifard M, Pashaiefar H, Yaghmaie M, et al. Expression Analysis of PVT1, CCDC26, and CCAT1 Long Noncoding RNAs in Acute Myeloid Leukemia Patients. Genet Test Mol Biomarkers.2018;22(10):593-598.
[48]Vaubel R,Kollmeyer T,Caron A,et al.Synchronous gemistocytic astrocytoma IDH-mutant and oligodendroglioma IDH-mutant and1p19q-codeleted in a patient with CCDC26 polymorphism. Acta Neuropathol. 2017;134(2):317-319.
[2]Stubbs B,Koyanagi A,Thompson T,et al. The epidemiology of back pain and its relationship with depression, psychosis, anxiety, sleep disturbances, and stress sensitivity:Data from 43 low-and middle-income countries. Gen Hosp Psychiatry.2016;43:63-70.
[3]Shmagel A, Foley Rand Ibrahim H. Epidemiology of Chronic Low Back Pain in US Adults:Data From the 2009-2010 National Health and Nutrition Examination Survey. Arthritis Care Res(Hoboken). 2016;68(11):1688-1694.
[4]Cheung KM,Karppinen J,Chan D, et al.Prevalence and pattern of lumbar magnetic resonance imaging changes in a population study of one thousand forty-three individuals. Spine(Phila Pa1976). 2009;34(9):934-940.
[5]Takatalo J,Karppinen J,Niinimaki J,et al. Does Lumbar Disc Degeneration on Magnetic Resonance Imaging Associate With Low Back Symptom Severity in Young Finnish Adults?.Spine.2011;36(25):2180-2189.
[6]Dario AB,Ferreira ML,Refshauge KM,et al.The relationship between obesity, low back pain, and lumbar disc degeneration when genetics and the environment are considered:a systematic review of twin studies.Spine J.2015;15(5):1106-1117.
[7]Battie MC,Videman T. Lumbar disc degeneration:Epidemiology and genetics. J Bone Joint Surg Am. 2006;88 Suppl 2:3-9.
[8]Tarnoki AD,Tarnoki DL,Kovacs DT,et al.Genetic relationship between obstructive sleep apnea and lumbar disc degeneration:results from a twin study. European Respiratory Journal. 2017; 50.
[9]Zhou X,Cheung CL,Karasugi T,et al.Trans-Ethnic Polygenic Analysis Supports Genetic Overlaps of Lumbar Disc Degeneration With Height, Body Mass Index, and Bone Mineral Density. Front Genet. 2018;9:267.
[10]Battie MC, Videman Tand Parent E. Lumbar disc degenerationEpidemiology and genetic influences. Spine.2004;29(23):2679-2690.
[11]Bjornsdottir G, Benonisdottir S, Sveinbjornsson G, et al. Sequence variant at 8q24.21 associates with sciatica caused by lumbar disc herniation. Nature Communications.2017, 8.
[12]Baldwin Aand Mesfin A. Adjacent Segment Disease 44 Years Following Posterior Spinal Fusion for Congenital Lumbar Kyphosis. Spine Deform.2017;5(6):435-439.
[13]Dong L,Xu Z,Chen X,et al.The change of adjacent segment after cervical disc arthroplasty compared with anterior cervical discectomy and fusion:a meta-analysis of randomized controlled trials. Spine J.2017;17(10):1549-1558.
[14]Arnbak B,Jensen RK,Manniche C,et al.Identification of subgroups of inflammatory and degenerative MRI findings in the spine and sacroiliac joints:a latent class analysis of 1037 patients with persistent low back pain.Arthritis Res Ther.2016;18(1):237.
[15]Muriuki MG, Havey RM,Voronov LI,et al. Effects of motion segment level, Pfirrmann intervertebral disc degeneration grade and gender on lumbar spine kinematics.J Orthop Res.2016;34(8):1389-1398.
[16]Xiao L,Ni CL,Shi JD,et al.Analysis of Correlation Between Vertebral Endplate Change and Lumbar Disc Degeneration.Medical Science Monitor.2017;23:4932-4938.
[17]Wu B,Meng C,Wang H,et al.Changes of proteoglycan and collagen II of the adjacent intervertebral disc in the cervical instability models. Biomed Pharmacother.2016; 84:754-758.
[18]Grant MP,Epure LM,Bokhari R,et al.Human cartilaginous endplate degeneration is induced by calcium and the extracellular calcium-sensing receptor in the intervertebral disc. Eur Cell Mater.2016;32:137-151.
[19]Xu HG,Zheng Q,Song JX,et al.Intermittent cyclic mechanical tension promotes endplate cartilage degeneration via canonical Wnt signaling pathway and E-cadherin/beta-catenin complex cross-talk. Osteoarthritis Cartilage. 2016;24(1):158-168.
[20]Sivan SS, Hayes AJ, Wachtel E, et al. Biochemical composition and turnover of the extracellular matrix of the normal and degenerate intervertebral disc. Eur Spine J.2014;23 Suppl 3:S344-53.
[21]Garnero P. The Role of Collagen Organization on the Properties of Bone. Calcif Tissue Int. 2015,97(3):229-240.
[22]张学利,宋海峰,朱如森,等.Ⅸ型胶原蛋白A2基因多态性与环境因素在腰椎间盘退变疾病中的作用[J]中华实验外科杂志,2017, 34(7):1232-1235.
[23]Wu HH, Wang ST, Chen WY, et al. Collagen IX gene polymorphisms and lumbar disc degeneration:a systematic review and meta-analysis. J Orthop Surg Res. 2018;13(1):47.
[24]Mio F, Chiba K, Hirose Y, et al. A functional polymorphism in COL11A1, which encodes the alpha 1 chain of type XI collagen, is associated with susceptibility to lumbar disc herniation[J]. Am J Hum Genet.2007;81(6):1271-1277.
[25]Ruel N, Markova DZ,Adams SL,et al.Fibronectin fragments and the cleaving enzyme ADAM-8 in the degenerative human intervertebral disc.Spine(Phila Pa 1976).2014; 39(16):1274-1279.
[26]Urano T,Narusawa K,Shiraki M,et al.Single-nucleotide polymorphism in the hyaluronan and proteoglycan link protein 1(HAPLN1)gene is associated with spinal osteophyte formation and disc degeneration in Japanese women. Eur Spine J.2011;20(4):572-577.
[27]S M H, M K S, G K C, et al. Association of CILP, COL9A2 and MMP3 Gene Polymorphisms with Lumbar Disc Degeneration in an Indian Population.J Mol Neurosci.2018;66(3):378-382.
[28]Li Y, Li K, Han XG, et al. The imbalance between TIMP3 and matrix-degrading enzymes plays an important role in intervertebral disc degeneration. Biochemical and Biophysical Research Communications, 2016, 469(3):507-514.
[29]张博,杨少华,林世洲,等.基质金属蛋白酶1在不同程度退变腰椎间盘髓核与纤维环中的表达及意义[J].中国组织工程研究, 2012,16(13):2346-2349.
[30]Deng B, Ren JZ, Meng XQ, et al. Expression profiles of MMP-1and TIMP-1 in lumbar intervertebral disc degeneration. Genet Mol Res.2015;14(4):19080-19086.
[31]Yuan HY, Tang Y, Lei L, et al.[Synergistic interaction between MMP-3, VDR gene polymorphisms and occupational risk factors on lumbar disc degeneration]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi.2010;28(5):334-338.
[32]Williams FMK, Bansal AT, van Meurs JB, et al. Novel genetic variants associated with lumbar disc degeneration in northern Europeans:a meta-analysis of 4600 subjects. Annals of the Rheumatic Diseases, 2013, 72(7):1141-1148.
[33]Lin WP,Lin JH,Chen XW,et al.Interleukin-10 promoter polymorphisms associated with susceptibility to lumbar disc degeneration in a Chinese cohort.Genet Mol Res.2011;10(3):1719-1727.
[34]Omair A,Lie BA,Reikeras O, et al. An Association Study of Interleukin 18 Receptor Genes(IL18R1 and IL18RAP)in Lumbar Disc Degeneration. Open Orthop J.2012; 6:164-171.
[35]Jiang H, Qin Z,Zong S,et al. Vitamin D receptor gene polymorphisms and lumbar disc degeneration:a systematic review and meta-analysis. Eur Spine J.2017;26(1):267-277.
[36]Zawilla NH, Darweesh H, Mansour N,et al. Matrix metalloproteinase-3, vitamin D receptor gene polymorphisms, and occupational risk factors in lumbar disc degeneration. J Occup Rehabil.2014; 24(2):370-381.
[37]Yuan HY,Tang Y,Liang YX,et al.Matrix metalloproteinase-3 and vitamin d receptor genetic polymorphisms, and their interactions with occupational exposure in lumbar disc degeneration. J Occup Health.2010;52(1):23-30.
[38]Schultz DR,Harrington WJ Jr.. Apoptosis:Programmed cell death at a molecular level. Semin Arthritis Rheum. 2003;32(6):345-369.
[39]Ariga K,Yonenobu K,Nakase T,et al.Mechanical stress-induced apoptosis of endplate chondrocytes in organ-cultured mouse intervertebral discs-An ex vivo study.Spine.2003; 28(14):1528-1533.
[40]Sakai D, Nakamura Y, Nakai T, et al. Exhaustion of nucleus pulposus progenitor cells with ageing and degeneration of the intervertebral disc. Nat Commun.2012;3:1264.
[41]Jiang M, Zhu K, Grenet J, et al.Retinoic acid induces caspase-8transcription via phospho-CREB and increases apoptotic responses to death stimuli in neuroblastoma cells. Biochim Biophys Acta. 2008;1783(6):1055-1067.
[42]Wang X, Luo T, Ruan M, et al. Association of the CCDC26rs4295627 polymorphism with the risk of glioma:Evidence from7,290 cases and 11,630 controls. Mol Clin Oncol.2016;4(5):878-882.
[43]Cao K, Li M, Miao J, et al. CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.Am J Transl Res.2018;10(1):274-282.
[44]Zeng J, Luo Y, Yu M, et al.CCDC26 rs4295627 polymorphisms associated with an increased risk of glioma:A meta-analysis. Adv Clin Exp Med.2017; 26(8):1275-1281.
[45]Peng Wand Jiang A.Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. Biomed Pharmacother.2016;83:712-717.
[46]Wang SL, Hui YZ, Li XM, et al. Silencing of lncRNA CCDC26Restrains the Growth and Migration of Glioma Cells In Vitro and In Vivo via Targeting miR-203.Oncology Res.2018; 26(8):1143-1154.
[47]Izadifard M, Pashaiefar H, Yaghmaie M, et al. Expression Analysis of PVT1, CCDC26, and CCAT1 Long Noncoding RNAs in Acute Myeloid Leukemia Patients. Genet Test Mol Biomarkers.2018;22(10):593-598.
[48]Vaubel R,Kollmeyer T,Caron A,et al.Synchronous gemistocytic astrocytoma IDH-mutant and oligodendroglioma IDH-mutant and1p19q-codeleted in a patient with CCDC26 polymorphism. Acta Neuropathol. 2017;134(2):317-319.