دوره 31، شماره 147 - ( 5-1402 )                   جلد 31 شماره 147 صفحات 390-381 | برگشت به فهرست نسخه ها


XML English Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Jumaah Fadhil Z, Abdul- Hassan Abbas A, Hadi Al-Osami M. The Influence of TNFRSF1B, PADI4, and miRNA 499 Gene Polymorphisms on Susceptibility and Responsiveness to TNF Inhibitors in Patients with Rheumatoid Arthritis. J Adv Med Biomed Res 2023; 31 (147) :381-390
URL: http://journal.zums.ac.ir/article-1-7316-fa.html
The Influence of TNFRSF1B, PADI4, and miRNA 499 Gene Polymorphisms on Susceptibility and Responsiveness to TNF Inhibitors in Patients with Rheumatoid Arthritis. Journal of Advances in Medical and Biomedical Research. 1402; 31 (147) :381-390

URL: http://journal.zums.ac.ir/article-1-7316-fa.html


چکیده:   (1315 مشاهده)

Background and Objective: Rheumatoid arthritis (RA) is a systemic autoimmune disease that causes joint deterioration. Over the past decade, the primary approach to treat RA has relied on biological medications. Despite confirming the effectiveness of this therapy, patients have shown significant diversity in their clinical responses to treatment. This variability can be attributed to various genetic polymorphisms that influence the response to biological drugs. This study was conducted to investigate whether TNFRSF1B (rs1061622), PADI4 (rs1748033), and miRNA 499 (rs3746444) gene polymorphisms are associated with susceptibility and responsiveness to TNF-α inhibitors in RA patients.
Materials and Methods: 100 RA patients (50 responders and 50 non-responders) and 100 apparently healthy subjects as the control group were studied. Genotyping of the polymorphisms was carried out using real-time polymerase chain reaction (PCR) with the TaqMan allelic discrimination assay.
Results: The frequency of TG (P0.039) and GG genotypes of TNFRSF1B (rs1061622) were higher in RA patients than in the control group. At the alleles level the mutant G allele was significantly more frequent among patients than control group (P=0.018). For PADI4 (rs1748033), the mutant C allele was more frequent among patients than controls (P=0.041). Sub-dividing of patients into responders and non-responders revealed that the mutant homozygous CC genotype of PADI4 (rs1748033) was significantly more frequent in non-responders than responders patients (P=0.046). AG genotype (P=0.016) and G allele (P=0.036) of miRNA 499a (rs3746444) were more frequent in non-responders than responders.
Conclusion: Variant genotypes of TNFRII (Rs1061622) and PADI4 (rs1748033), may be associated with an increased risk of RA while PADI4 (rs1748033) and miRNA-499a (rs3746444) polymorphism may be associated with non-response to infliximab.

متن کامل [PDF 424 kb]   (575 دریافت)    
نوع مطالعه: مقاله پژوهشی | موضوع مقاله: Medical Biology
دریافت: 1402/4/16 | پذیرش: 1402/6/18 | انتشار: 1402/7/5

فهرست منابع
1. Clunie G, Wilkinson N, Nikiphorou E, Jadon D. Oxford handbook of rheumatology: Oxford University Press; 2018. [DOI:10.1093/med/9780198728252.001.0001]
2. Radner H, Smolen JS, Aletaha D. Remission in rheumatoid arthritis: benefit over low disease activity in patient-reported outcomes and costs. Arthritis Res Ther. 2014;16(1):R56. [DOI:10.1186/ar4491] [PMID] [PMCID]
3. Constantin A, Dieudé P, Lauwers-Cancès V, Jamard B, Mazières B, Cambon-Thomsen A, et al. Tumor necrosis factor receptor II gene polymorphism and severity of rheumatoid arthritis. Arthritis Rheumatol. 2004;50(3):742-7. [DOI:10.1002/art.20113] [PMID]
4. Barton A, Worthington J. Genetic susceptibility to rheumatoid arthritis: an emerging picture. Arthritis Rheum. 2009;61(10):1441-6. [DOI:10.1002/art.24672] [PMID]
5. Aminikhoo MH, Pak F, Ahmadi K, Barati M, Fasihi M, Nejad ZR, et al. Association study of tumor necrosis factor receptor type II polymorphism (196R) with rheumatoid arthritis in Iranian people. Middle East j Rehabil Health Stud. 2020;7(1):1-5. [DOI:10.5812/mejrh.88078]
6. Pallio G, Mannino F, Irrera N, Eid AH, Squadrito F, Bitto A. Polymorphisms involved in response to biological agents used in rheumatoid arthritis. Biomolecules. 2020;10(9):1203. [DOI:10.3390/biom10091203] [PMID] [PMCID]
7. Luo Y, Arita K, Bhatia M, Knuckley B, Lee Y-H, Stallcup MR, et al. Inhibitors and Inactivators of Protein Arginine Deiminase 4:  Functional and Structural Characterization. Biochemistry. 2006;45(39):11727-36. [DOI:10.1021/bi061180d] [PMID] [PMCID]
8. Vossenaar ER, Zendman AJW, van Venrooij WJ. Citrullination, a possible functional link between susceptibility genes and rheumatoid arthritis. Arthritis Res Ther. 2003;6(1):1. [DOI:10.1186/ar1027] [PMID] [PMCID]
9. Guo S, Chang C, Xu L, Zhang R, Jin Y, Xiong M, et al. Epigenetic regulation mediated by microRNAs in the susceptibility and pathogenesis of rheumatoid arthritis: Preprints; 2020. [DOI:10.20944/preprints202004.0241.v2]
10. Giurgiu M, Kaltenbach R, Ahrend F, Weeks S, Clifton H, Bouldo M, et al. Multiple Genetic Polymorphisms within microRNA Targets and Homologous microRNA-Binding Sites: Two More Factors Influencing microRNA-Mediated Regulation of Gene Expression. Advances in Genetic Polymorphisms. London, United Kingdom: IntechOpen; 2023. [DOI:10.5772/intechopen.1002250]
11. Cohen S, Emery P. The American College of Rheumatology/European League Against Rheumatism Criteria for the classification of rheumatoid arthritis: a game changer. Ann Rheum Dis. 2010;69:1575-6. [DOI:10.1136/ard.2010.138446] [PMID]
12. Canhão H, Rodrigues AM, Gregório MJ, Dias SS, Melo Gomes JA, Santos MJ, et al. Common evaluations of disease activity in rheumatoid arthritis reach discordant classifications across different populations. Front Med. 2018;5:40. [DOI:10.3389/fmed.2018.00040] [PMID] [PMCID]
13. Dieudé P, Cornélis F. Genetic basis of rheumatoid arthritis. Jt Bone Spine. 2005;72(6):520-6. [DOI:10.1016/j.jbspin.2005.09.001] [PMID]
14. Canet LM, Filipescu I, Cáliz R, Lupiañez CB, Canhão H, Escudero A, et al. Genetic variants within the TNFRSF1B gene and susceptibility to rheumatoid arthritis and response to anti-TNF drugs: a multicenter study. Pharmacogenet Genomics. 2015;25(7):323-33. [DOI:10.1097/FPC.0000000000000140] [PMID]
15. Xie X, Li F, Chen J, Gao J, Lu F. Association of TNFRSF1B+ 676 gene polymorphism with the risk of rheumatoid arthritis in Han Chinese population in Hunan. Zhong nan da xue xue bao Yi xue ban= J Cent South Univ Med Sci. 2016;41(9):891-7.
16. Cornélis F, Fauré S, Martinez M, Prud'homme J-F, Fritz P, Dib C, et al. New susceptibility locus for rheumatoid arthritis suggested by a genome-wide linkage study. Proc Natl Acad Sci. 1998;95(18):10746-50. [DOI:10.1073/pnas.95.18.10746] [PMID] [PMCID]
17. Ticha O, Moos L, Wajant H, Bekeredjian-Ding I. Expression of Tumor Necrosis Factor Receptor 2 Characterizes TLR9-Driven Formation of Interleukin-10-Producing B Cells. Front Immunol. 2018;8:1951. [DOI:10.3389/fimmu.2017.01951] [PMID] [PMCID]
18. Ye L-L, Wei X-S, Zhang M, Niu Y-R, Zhou Q. The Significance of Tumor Necrosis Factor Receptor Type II in CD8+ Regulatory T Cells and CD8+ Effector T Cells. Front Immunol. 2018;9:583. [DOI:10.3389/fimmu.2018.00583] [PMID] [PMCID]
19. Shaker OG, El Boghdady NA, El Sayed AE. Association of MiRNA-146a, MiRNA-499, IRAK1 and PADI4 Polymorphisms with Rheumatoid Arthritis in Egyptian Population. Cell Physiol Biochem. 2018;46(6):2239-49. [DOI:10.1159/000489592] [PMID]
20. Suzuki A, Yamada R, Chang X, Tokuhiro S, Sawada T, Suzuki M, et al. Functional haplotypes of PADI4, encoding citrullinating enzyme peptidylarginine deiminase 4, are associated with rheumatoid arthritis. Nat Genet. 2003;34(4):395-402. [DOI:10.1038/ng1206] [PMID]
21. Hashemi M, Zakeri Z, Taheri H, Bahari G, Taheri M. Association between Peptidylarginine Deiminase Type 4 rs1748033 Polymorphism and Susceptibility to Rheumatoid Arthritis in Zahedan, Southeast Iran. Iran J Allergy Asthma Immunol. 2015;14(3):255-60.
22. Kang CP, Lee H-S, Ju H, Cho H, Kang C, Bae S-C. A functional haplotype of the PADI4 gene associated with increased rheumatoid arthritis susceptibility in Koreans. Arthritis Rheumatol. 2006;54(1):90-6. [DOI:10.1002/art.21536] [PMID]
23. Hoppe B, Häupl T, Gruber R, Kiesewetter H, Burmester GR, Salama A, et al. Detailed analysis of the variability of peptidylarginine deiminase type 4 in German patients with rheumatoid arthritis: a case-control study. Arthritis Res Ther. 2006;8: R34. [DOI:10.1186/ar1889] [PMID] [PMCID]
24. Yang B, Zhang JL, Shi YY, Li DD, Chen J, Huang ZC, et al. Association study of single nucleotide polymorphisms in pre-miRNA and rheumatoid arthritis in a Han Chinese population. Mol Biol Rep. 2011;38(8):4913-9. [DOI:10.1007/s11033-010-0633-x] [PMID]
25. Hashemi M, Eskandari-Nasab E, Zakeri Z, Atabaki M, Bahari G, Jahantigh M, et al. Association of pre-miRNA-146a rs2910164 and pre miRNA-499 rs3746444 polymorphisms and susceptibility to rheumatoid arthritis. Mol Med Rep. 2013;7(1):287-91. [DOI:10.3892/mmr.2012.1176] [PMID]
26. Ayeldeen G, Nassar Y, Ahmed H, Shaker O, Gheita T. Possible use of miRNAs-146a and -499 expression and their polymorphisms as diagnostic markers for rheumatoid arthritis. Mol Cell Biochem. 2018;449(1-2):145-56. [DOI:10.1007/s11010-018-3351-7] [PMID]
27. Ali Y, Chen Y, Islam ZU, Aman A, Almutairi MM, Alouffi A, et al. MIR149 rs2292832 and MIR499 rs3746444 Genetic Variants Associated with the Risk of Rheumatoid Arthritis. Genes. 2023;14(2):431. [DOI:10.3390/genes14020431] [PMID] [PMCID]
28. Vasilopoulos Y, Bagiatis V, Stamatopoulou D, Zisopoulos D, Alexiou I, Sarafidou T, et al. Association of anti-CCP positivity and carriage of TNFRII susceptibility variant with anti-TNF-α response in rheumatoid arthritis. Clin Exp Rheumatol. 2011;29(4):701-4.
29. Fabris M, Tolusso B, Poi ED, Assaloni R, Sinigaglia L, Ferraccioli G. Tumor necrosis factor-alpha receptor II polymorphism in patients from southern Europe with mild-moderate and severe rheumatoid arthritis. J Rheumatol. 2002;29(9):1847-50.
30. Bagheri-Hosseinabadi Z, Mirzaei MR, Esmaeili O, Asadi F, Ahmadinia H, Shamsoddini B, et al. Implications of Peptidyl Arginine Deiminase 4 gene transcription and polymorphisms in susceptibility to rheumatoid arthritis in an Iranian population. BMC Medical Genom. 2023;16(1):104. [DOI:10.1186/s12920-023-01532-9] [PMID] [PMCID]

بازنشر اطلاعات
Creative Commons License این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است.

کلیه حقوق این وب سایت متعلق به Journal of Advances in Medical and Biomedical Research می باشد.

طراحی و برنامه نویسی : یکتاوب افزار شرق

© 2024 CC BY-NC 4.0 | Journal of Advances in Medical and Biomedical Research

Designed & Developed by : Yektaweb