The Investigation of Lectin-Like Oxidized LDL Receptor 1 (LOX-1) K167N Polymorphism, Inflammation, and Lipid Status in Patients with Coronary Artery Bypass Grafting

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Nurten Bahtiyar
Onur Baykara
Yalcın Hacıoglu
Tuba Oner
Fatma Behice Cinemre
Birsen Aydemir
Ilhan Onaran
Caner Aslan
Cigdem Tel
Rauf Hamid
Berk Arapi
Ali Riza Kiziler
Gonul Kanigur

Abstract

Objective: Coronary artery disease (CAD) is a pathological condition resulting from atherosclerosis in the coronary arteries. Besides traditional risk factors, genetic factors such as single nucleotide polymorphs (SNPs) can be involve in disease process. Inflammation plays a role in pathological changes throughout atherosclerosis, from initiation to progress. In this study, we aimed to evaluate the effects of lectin-like oxidized LDL receptor 1 (LOX-1) K167N polymorphism, inflammation, and lipid status in patients with coronary artery bypass grafting (CABG).


Material and Methods: The study population consisted of 129 CAD patients who had undergone CABG, and 71 healthy controls. The LOX-1 K167N polymorphism was genotyped using PCR-RFLP technique. Plasma interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-33 (IL-33) levels were determined by enzyme-linked immunosorbent assay (ELISA) kits.


Results: The distribution of the LOX-1 K167N genotypes and alleles did not differ significantly between CAD patients with CABG and controls. There were no significant differences in plasma IL-1β, TNF- α, IL-33, HDL-C, and LDL-C levels between the patients and controls.  IL-1β and systolic blood pressure values were significantly higher in KK genotype patients compared to the same genotype controls(P<0.05). Similarly, systolic blood pressures were higher in NK genotype patients compared with NK genotype controls (P<0.01).


Conclusions: IL-1β and systolic blood pressure values were found to be higher in post CABG CAD patients with the KK genotype compared to healthy controls with the same genotype while inflammatory markers and lipid profiles selected according to LOX-1 K167N polymorphism genotype and allele distributions did not differ between groups. Although we couldn’t find an assocation between LOX-1 K167N polymorphism and CAD other than high BP in our study, studies  with larger sample sizes might reveal such a relation.

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How to Cite
Bahtiyar, N., Baykara, O., Hacıoglu, Y., Oner, T., Cinemre, F. B., Aydemir, B. ., Onaran, I., Aslan, C., Tel, C., Hamid, R., Arapi, B., Kiziler, A. R., & Kanigur, G. (2023). The Investigation of Lectin-Like Oxidized LDL Receptor 1 (LOX-1) K167N Polymorphism, Inflammation, and Lipid Status in Patients with Coronary Artery Bypass Grafting. Medical Science and Discovery, 10(6), 400–405. https://doi.org/10.36472/msd.v10i6.961
Section
Research Article
Received 2023-05-26
Accepted 2023-06-19
Published 2023-06-19

References

Knuuti J, Wijns W, Saraste A et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes: the Task Force for the diagnosis and management of chronic coronary syndromes of the European Society of Cardiology (ESC). Eur. Heart J. 2020; 41: 407-477.

Hajar R. Risk factors for coronary artery disease: historical perspectives. Heart views. 2017; 18: 109.

Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat. Rev. Genet. 2017; 18: 331-344.

Boren J, Chapman MJ, Krauss RM et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur. Heart J. 2020; 41: 2313-2330.

Chen X-p, Du G-h. Lectin-like oxidized low-density lipoprotein receptor-1: protein, ligands, expression and pathophysiological significance. Chin. Med. J. 2007; 120: 421-426.

Recep E, Bayoglu B, Arslan C et al. Roles of OLR1 and IL17A variants on clinical phenotypes of Turkish patients undergoing coronary artery bypass surgery. Turkish J. Biochem. 2022; 47: 571-579.

Malakar AK, Choudhury D, Halder B et al. A review on coronary artery disease, its risk factors, and therapeutics. J. Cell. Physiol. 2019; 234: 16812-16823.

Wang Q. Molecular genetics of coronary artery disease. Opin. Cardiol. 2005; 20: 182.

Ozaki K, Tanaka T. Molecular genetics of coronary artery disease. J. Hum. Genet. 2016; 61: 71-77.

Pranavchand R, Reddy B. Current status of understanding of the genetic etiology of coronary heart disease. J. Postgrad. Med. 2013; 59: 30.

Liu H, Liu W, Liao Y et al. CADgene: a comprehensive database for coronary artery disease genes. Nucleic Acids Res. 2011; 39: D991-D996.

Biocca S, Falconi M, Filesi I et al. Functional analysis and molecular dynamics simulation of LOX-1 K167N polymorphism reveal alteration of receptor activity. Plos one 2009; 4: e4648.

Hattori H, Sonoda A, Sato H et al. G501C polymorphism of oxidized LDL receptor gene (OLR1) and ischemic stroke. Brain Res. 2006; 1121: 246-249.

Mango R, Clementi F, Borgiani P et al. Association of single nucleotide polymorphisms in the oxidised LDL receptor 1 (OLR1) gene in patients with acute myocardial infarction. J. Med. Genet. 2003; 40: 933-936.

Kurnaz O, Aydoğan HY, Isbir CS et al. Is LOX-1 K167N polymorphism protective for coronary artery disease? In Vivo. 2009; 23: 969-973.

Tatsuguchi M, Furutani M, Hinagata J-i et al. Oxidized LDL receptor gene (OLR1) is associated with the risk of myocardial infarction. Biochem. Biophys. Res. Commun. 2003; 303: 247-250.

Zhang J, Yin C, Zhang Y et al. The role of OLR1 polymorphisms in determining the risk and prognosis of ischemic stroke in a Chinese population. NeuroRehabilitation 2013; 32: 391-396.

Sakowicz A, Fendler W, Lelonek M, Pietrucha T. Original research Genetic variability and the risk of myocardial infarction in Poles under 45 years of age. Arch. Med. Sci. 2010; 6: 160-167.

Ohmori R, Momiyama Y, Nagano M et al. An oxidized low‐density lipoprotein receptor gene variant is inversely associated with the severity of coronary artery disease. Clin. Cardiol. 2004; 27: 641-644.

Trabetti E, Biscuola M, Cavallari U et al. On the association of the oxidised LDL receptor 1 (OLR1) gene in patients with acute myocardial infarction or coronary artery disease. Eur. J. Hum. Genet. 2006; 14: 127-130.

Morgan TM, Krumholz HM, Lifton RP, Spertus JA. Nonvalidation of reported genetic risk factors for acute coronary syndrome in a large-scale replication study. Jama 2007; 297: 1551-1561.

Knowles JW, Assimes TL, Boerwinkle E et al. Failure to replicate an association of SNPs in the oxidized LDL receptor gene (OLR1) with CAD. BMC Med. Genet. 2008; 9: 1-11.

Puccetti L, Pasqui A, Bruni F et al. Lectin-like oxidized-LDL receptor-1 (LOX-1) polymorphisms influence cardiovascular events rate during statin treatment. Int. J. Cardiol. 2007; 119: 41-47.

Salehipour P, Rezagholizadeh F, Mahdiannasser M et al. Association of OLR1 gene polymorphisms with the risk of coronary artery disease: A systematic review and meta-analysis. Heart & Lung 2021; 50: 334-343.

Galkina E, Ley K. Immune and inflammatory mechanisms of atherosclerosis. Annu. Rev. Immunol. 2009; 27.

Fatkhullina A, Peshkova I, Koltsova E. The role of cytokines in the development of atherosclerosis. Biochem. (Mosc.). 2016; 81: 1358-1370.

Kirii H, Niwa T, Yamada Y et al. Lack of interleukin-1β decreases the severity of atherosclerosis in ApoE-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2003; 23: 656-660.

McLaren JE, Michael DR, Salter RC et al. IL-33 reduces macrophage foam cell formation. J. Immun. 2010; 185: 1222-1229.

Miller AM, Xu D, Asquith DL et al. IL-33 reduces the development of atherosclerosis. J. Exp. Med. 2008; 205: 339-346.

Gu YJ, Mariani MA, van Oeveren PhD W et al. Reduction of the inflammatory response in patients undergoing minimally invasive coronary artery bypass grafting. Ann. Thorac. Surg. 1998; 65: 420-424.