Polymorphism rs7079 in miR-31/-584 Binding Site in Angiotensinogen Gene Associates with Earlier Onset of Coronary Artery Disease in Central European Population
Language English Country Switzerland Media electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
36360218
PubMed Central
PMC9690213
DOI
10.3390/genes13111981
PII: genes13111981
Knihovny.cz E-resources
- Keywords
- age, angiotensinogen, coronary artery disease, restenosis, rs7079,
- MeSH
- 3' Untranslated Regions MeSH
- Angiotensinogen genetics MeSH
- Humans MeSH
- MicroRNAs * genetics metabolism MeSH
- Coronary Artery Disease * genetics MeSH
- Polymorphism, Genetic MeSH
- Binding Sites MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 3' Untranslated Regions MeSH
- AGT protein, human MeSH Browser
- Angiotensinogen MeSH
- MicroRNAs * MeSH
- MIRN31 microRNA, human MeSH Browser
Angiotensinogen (AGT) represents a key component of the renin-angiotensin-aldosterone system (RAAS). Polymorphisms in the 3' untranslated region (3'UTR) of the AGT gene may alter miRNA binding and cause disbalance in the RAAS. Within this study, we evaluated the possible association of AGT +11525C/A (rs7079) with the clinical characteristics of patients with coronary artery diseases (CAD). Selective coronarography was performed in 652 consecutive CAD patients. Clinical characteristics of the patients, together with peripheral blood samples for DNA isolation, were collected. The genotyping of rs7079 polymorphism was performed with TaqMan® SNP Genotyping Assays. We observed that patients with the CC genotype were referred for coronarography at a younger age compared to those with the AA+CA genotypes (CC vs. AA+CA: 59.1 ± 9.64 vs. 60.91 ± 9.5 (years), p = 0.045). Moreover, according to the logistic regression model, patients with the CC genotype presented more often with restenosis than those with the CA genotype (p = 0.0081). In conclusion, CC homozygotes for rs7079 present with CAD symptoms at a younger age compared with those with the AA+CA genotype, and they are more prone to present with restenosis compared with heterozygotes.
Department of Physiology Faculty of Medicine Masaryk University 625 00 Brno Czech Republic
International Clinical Research Center St Anne's University Hospital 656 91 Brno Czech Republic
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Benigni A., Cassis P., Remuzzi G. Angiotensin II revisited: New roles in inflammation, immunology and aging. EMBO Mol. Med. 2010;2:247–257. doi: 10.1002/emmm.201000080. PubMed DOI PMC
Silva G.M., França-Falcão M.S., Calzerra N.T.M., Luz M.S., Gadelha D.D.A., Balarini C.M., Queiroz T.M. Role of Renin-Angiotensin System Components in Atherosclerosis: Focus on Ang-II, ACE2, and Ang-1-7. Front. Physiol. 2020;11:1067. doi: 10.3389/fphys.2020.01067. PubMed DOI PMC
Furuya K., Yamaguchi E., Itoh A., Hizawa N., Ohnuma N., Kojima J., Kodama N., Kawakami Y. Deletion polymorphism in the angiotensin I converting enzyme (ACE) gene as a genetic risk factor for sarcoidosis. Thorax. 1996;51:777–780. doi: 10.1136/thx.51.8.777. PubMed DOI PMC
White P.C., Slutsker L. Haplotype analysis of CYP11B2. Endocr. Res. 1995;21:437–442. doi: 10.3109/07435809509030459. PubMed DOI
Slaby O., Bienertova-Vasku J., Svoboda M., Vyzula R. Genetic polymorphisms, and microRNAs: New direction in molecular epidemiology of solid cancer. J. Cell. Mol. Med. 2012;16:8–21. doi: 10.1111/j.1582-4934.2011.01359.x. PubMed DOI PMC
Mopidevi B., Ponnala M., Kumar A. Human angiotensinogen +11525 C/A polymorphism modulates its gene expression through microRNA binding. Physiol. Genom. 2013;45:901–906. doi: 10.1152/physiolgenomics.00056.2013. PubMed DOI PMC
Machal J., Novak J., Hezova R., Zlamal F., Vasku A., Slaby O., Bienertova-Vasku J. Polymorphism in miR-31 and miR-584 binding site in the angiotensinogen gene differentially influences body fat distribution in both sexes. Genes Nutr. 2015;10:488. doi: 10.1007/s12263-015-0488-9. PubMed DOI PMC
Wu Y., Wang M., Zhang J., Sun N., Li C. A new model of the mechanism underlying lead poisoning: SNP in miRNA target region influence the AGT expression level. Hereditas. 2019;156:6. doi: 10.1186/s41065-019-0084-x. PubMed DOI PMC
Máchal J., Vašků A., Kincl V., Hlavna M., Bartáková V., Jurajda M., Meluzín J. Association between three single nucleotide polymorphisms in eotaxin (CCL 11) gene, hexanucleotide repetition upstream, severity and course of coronary atherosclerosis. J. Appl. Genet. 2012;53:271–278. doi: 10.1007/s13353-012-0104-2. PubMed DOI
Bartel D.P. MicroRNAs: Genomics, biogenesis, mechanism, and function. Cell. 2004;116:281–297. doi: 10.1016/S0092-8674(04)00045-5. PubMed DOI
Al-Najai M., Muiya P., Tahir A.I., Elhawari S., Gueco D., Andres E., Mazhar N., Altassan N., Alshahid M., Dzimiri N. Association of the angiotensinogen gene polymorphism with atherosclerosis and its risk traits in the Saudi population. BMC Cardiovasc. Disord. 2013;13:17. doi: 10.1186/1471-2261-13-17. PubMed DOI PMC
Ono M., Ochi T., Munekage K., Ogasawara M., Hirose A., Nozaki Y., Takahashi M., Okamoto N., Saibara T. Angiotensinogen gene haplotype is associated with the prevalence of Japanese non-alcoholic steatohepatitis. Hepatol. Res. Off. J. Jpn. Soc. Hepatol. 2011;41:1223–1229. doi: 10.1111/j.1872-034X.2011.00883.x. PubMed DOI
Wang H.-W., Huang T.-S., Lo H.-H., Huang P.-H., Lin C.-C., Chang S.-J., Liao K.-H., Tsai C.-H., Chan C.-H., Tsai C.-F., et al. Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 2014;34:857–869. doi: 10.1161/ATVBAHA.113.303001. PubMed DOI
Weber M., Baker M.B., Patel R.S., Quyyumi A.A., Bao G., Searles C.D. MicroRNA Expression Profile in CAD Patients and the Impact of ACEI/ARB. Cardiol. Res. Pract. 2011;2011:532915. doi: 10.4061/2011/532915. PubMed DOI PMC
Jiang F., Li J., Wu G., Miao Z., Lu L., Ren G., Wang X. Upregulation of microRNA-335 and microRNA-584 contributes to the pathogenesis of severe preeclampsia through downregulation of endothelial nitric oxide synthase. Mol. Med. Rep. 2015;12:5383–5390. doi: 10.3892/mmr.2015.4018. PubMed DOI
Kim S., Lee K.-S., Choi S., Kim J., Lee D.-K., Park M., Park W., Kim T.-H., Hwang J.Y., Won M.-H., et al. NF-κB–responsive miRNA-31-5p elicits endothelial dysfunction associated with preeclampsia via down-regulation of endothelial nitric-oxide synthase. J. Biol. Chem. 2018;293:18989–19000. doi: 10.1074/jbc.RA118.005197. PubMed DOI PMC
Navarro E., Mallén A., Cruzado J.M., Torras J., Hueso M. Unveiling ncRNA regulatory axes in atherosclerosis progression. Clin. Transl. Med. 2020;9:5. doi: 10.1186/s40169-020-0256-3. PubMed DOI PMC
Buccheri D., Piraino D., Andolina G., Cortese B. Understanding and managing in-stent restenosis: A review of clinical data, from pathogenesis to treatment. J. Thorac. Dis. 2016;8:E1150–E1162. doi: 10.21037/jtd.2016.10.93. PubMed DOI PMC
Suárez Y., Wang C., Manes T.D., Pober J.S. TNF-induced miRNAs Regulate TNF-induced expression of E-Selectin and ICAM-1 on Human Endothelial Cells: Feedback Control of Inflammation. J. Immunol. Baltim. Md. 1950. 2010;184:21–25. doi: 10.4049/jimmunol.0902369. PubMed DOI PMC
Huang R., Chen X., Long Y., Chen R. MiR-31 promotes Th22 differentiation through targeting Bach2 in coronary heart disease. Biosci. Rep. 2019;39:BSR20190986. doi: 10.1042/BSR20190986. PubMed DOI PMC
Zhang L., Wang T., Wang X., Du R., Zhang K., Liu X., Ma D., Yu S., Su G., Li Z., et al. Elevated frequencies of circulating Th22 cell in addition to Th17 cell and Th17/Th1 cell in patients with acute coronary syndrome. PLoS ONE. 2013;8:e71466. doi: 10.1371/journal.pone.0071466. PubMed DOI PMC