Association between NF‑κBI and NF‑κBIA polymorphisms and coronary artery disease

Arslan,Serdal; Korkmaz,Özge; Özbilüm,Nil; Berkan,Öcal

doi:10.3892/br.2015.499

Association between NF‑κBI and NF‑κBIA polymorphisms and coronary artery disease

Authors:
- Serdal Arslan
- Özge Korkmaz
- Nil Özbilüm
- Öcal Berkan
View Affiliations

Affiliations: Department of Medical Biology, Cumhuriyet University, 58140 Sivas, Turkey, Department of Cardiovascular Surgery, Faculty of Medicine, Cumhuriyet University, 58140 Sivas, Turkey, Department of Molecular Biology and Genetics, Faculty of Science, Cumhuriyet University, 58140 Sivas, Turkey
Published online on: July 29, 2015 https://doi.org/10.3892/br.2015.499
Pages: 736-740

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

Coronary artery disease (CAD) is the leading cause of fatalities worldwide. Nuclear factor (NF)‑κB is a transcription factor that controls cell proliferation, differentiation and immunity. To the best of our knowledge, the present study is the first investigation of the association between CAD and NF‑κB1 ‑94 W/D/NF‑κBIA 3'‑untranslated region (3'‑UTR) A→G polymorphisms. The study population comprised 226 CAD patients and 201 controls. There was no significant difference in NF‑κB1A 3'‑UTR A→G in the allele and genotype frequencies between case and control populations. The D allele frequency of NF‑κB1 ‑94 in the case group was significantly higher compared to the control group (P=0.028, odds ratio=1.37). The genotype frequency of NF‑κB1 ‑94 DD in the case group was significantly higher compared to the controls (P=0.028). Linkage analysis showed a close linkage among these 2 genes (P<0.001 for case and control), and AD and GD haplotypes were associated with CAD (P<0.001; P=0.015, respectively). NF‑κB1 ‑94 DD genotype can be a significant risk factor for the development of CAD.

View Figures

View References

1	World Health Organization (WHO), . Prevention of Cardiovascular disease: Guidelines for assessment and management of cardiovascular risk. WHO Library; Geneva, Switzerland: 2007
2	Onat A, Yazıcı M, Sarı İ, Türkmen S, Uzunlar B and Uyarel H ve ark: TEKHARF 2003 yılı tarama takibi: ölüm ve koroner olaylara ilişkin sonuçlar şehirlilerde mortalitenin azaldığına işaret. Türk Kardiyol Dern Arş. 31:762–769. 2003.(In Turkish).
3	Ross R: Atherosclerosis - an inflammatory disease. N Eng J Med. 340:115–126. 1999. View Article : Google Scholar
4	O'Dea E and Hoffmann A: NF-κB signaling. Wiley Interdiscip Rev Syst Biol Med. 1:107–115. 2009. View Article : Google Scholar : PubMed/NCBI
5	Heron E, Deloukas P and Van Loon AP: The complete exon-intron structure of the 150-kb human gene NFKB1, which encodes p105 and p50 proteins of transcription factors NF-kappa B and I kappa B-gamma: Implications for NF-kappa B-mediated signal transduction. Genomics. 30:493–505. 1995. View Article : Google Scholar : PubMed/NCBI
6	Pereira SG and Oakley F: Nuclear factor-kappaB1: Regulation and function. Int J Biochem Cell Biol. 40:1425–1430. 2008. View Article : Google Scholar : PubMed/NCBI
7	Chiao PJ, Miyamoto S and Verma IM: Autoregulation of I kappa B alpha activity. Proc Natl Acad Sci USA. 91:28–32. 1994. View Article : Google Scholar : PubMed/NCBI
8	Baeuerle PA: IkappaB-NF-kappaB structures: At the interface of inflammation control. Cell. 95:729–731. 1998. View Article : Google Scholar : PubMed/NCBI
9	Arslan S and Engin A: Relationship between NF-κB1 and NF-κBIA genetic polymorphisms and Crimean-Congo hemorrhagic fever. Scand J Infect Dis. 44:138–143. 2012. View Article : Google Scholar : PubMed/NCBI
10	Yeh FC and Boyle TJB: Population genetic analysis of co-dominant and dominant markers and quantitative traits. Belgian Journal of Botany. 129:1571997.
11	Terwilliger JD and Ott J: A novel polylocus method for linkage analysis using the lod-score or affected sib-pair method. Genet Epidemiol. 10:477–482. 1993. View Article : Google Scholar : PubMed/NCBI
12	Romzova M, Hohenadel D, Kolostova K, et al: NF-κB and its inhibitor IκB in relation to type 2 diabetes and its microvascular and atherosclerotic complications. Hum Immunol. 67:706–713. 2006. View Article : Google Scholar : PubMed/NCBI
13	Curran JE, Weinstein SR and Griffiths LR: Polymorphic variants of NFKB1 and its inhibitory protein NFKBIA, and their involvement in sporadic breast cancer. Cancer Lett. 188:103–107. 2002. View Article : Google Scholar : PubMed/NCBI
14	Özbilüm N, Arslan S, Berkan Ö, Yanartaş M and Aydemir EI: The role of NF-κB1A promoter polymorphisms on coronary artery disease risk. Basic Clin Pharmacol Toxicol. 113:187–192. 2013. View Article : Google Scholar : PubMed/NCBI
15	Klein W, Tromm A, Folwaczny C, Hagedorn M, Duerig N, Epplen JT, Schmiegel WH and Griga T: Polymorphism of the NFKBIA gene is associated with Crohn's disease patients lacking a predisposing allele of the CARD15 gene. Int J Colorectal Dis. 19:153–156. 2004. View Article : Google Scholar : PubMed/NCBI
16	Parker KM, Ma MH, Manyak S, et al: Identification of polymorphisms of the IκBα gene associated with an increased risk of multiple myeloma. Cancer Genet Cytogenet. 137:43–48. 2002. View Article : Google Scholar : PubMed/NCBI
17	Lin CW, Hsieh YS, Hsin CH, et al: Effects of NFKB1 and NFKBIA gene polymorphisms on susceptibility to environmental factors and the clinicopathologic development of oral cancer. PLoS One. 7:e350782012. View Article : Google Scholar : PubMed/NCBI
18	Zhang P, Wei Q, Li X, et al: A functional insertion/deletion polymorphism in the promoter region of the NFKB1 gene increases susceptibility for prostate cancer. Cancer Genet Cytogenet. 191:73–77. 2009. View Article : Google Scholar : PubMed/NCBI
19	Liang M, Xu X, Gong Y, Tang Y and Lin L: Risk association between the NF-κB1 −94ins/delATTG promoter polymorphism and inflammatory bowel diseases: A meta-analysis. Dig Dis Sci. 57:2304–2309. 2012. View Article : Google Scholar : PubMed/NCBI
20	Zou YF, Wang F, Feng XL, Tao JH, Zhu JM, Pan FM and Su H: Association of NFKB1 −94ins/delATTG promoter polymorphism with susceptibility to autoimmune and inflammatory diseases: A meta-analysis. Tissue Antigens. 77:9–17. 2011. View Article : Google Scholar : PubMed/NCBI
21	Karban AS, Okazaki T, Panhuysen CI, et al: Functional annotation of a novel NFKB1 promoter polymorphism that increases risk for ulcerative colitis. Hum Mol Genet. 13:35–45. 2004. View Article : Google Scholar : PubMed/NCBI
22	Vogel U, Jensen MK, Due KM, et al: The NFKB1 ATTG ins/del polymorphism and risk of coronary heart disease in three independent populations. Atherosclerosis. 219:200–204. 2011. View Article : Google Scholar : PubMed/NCBI
23	Chen Z, Ma G, Qian Q, Yao Y, Feng Y and Tang C: Toll-like receptor 8 polymorphism and coronary artery disease. Mol Biol Rep. 36:1897–1901. 2009. View Article : Google Scholar : PubMed/NCBI
24	Hotamisligil GS: Inflammation and metabolic disorders. Nature. 444:860–867. 2006. View Article : Google Scholar : PubMed/NCBI
25	Elliott P, Chambers JC, Zhang W, et al: Genetic Loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA. 302:37–48. 2009. View Article : Google Scholar : PubMed/NCBI
26	ChaMolstad H, Agrawal A, Zhang D, Samols D and Kushner I: The Rel family member P50 mediates cytokine-induced C-reactive protein expression by a novel mechanism. J Immunol. 165:4592–4597. 2000. View Article : Google Scholar : PubMed/NCBI