TREML4 polymorphisms increase the mRNA in blood leukocytes in the progression of atherosclerosis

• Published in: Scientific reports Vol. 12; no. 1; p. 18612
• Main Authors: Duarte, Victor Hugo Rezende, Cruz, Marina Sampaio, Bertolami, Adriana, Hirata, Mario Hiroyuki, Hirata, Rosario Dominguez Crespo, Luchessi, André Ducati, Silbiger, Vivian Nogueira
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 03.11.2022; Nature Publishing Group; Nature Portfolio
• Subjects: 631/208; 631/337; 692/4019; 692/53; Alleles; Arteriosclerosis; Atherosclerosis; Atherosclerosis - complications; Atherosclerosis - genetics; Blood; Calcification (ectopic); Cardiovascular disease; Congestive heart failure; Coronary artery; Coronary Artery Disease - complications; Coronary Artery Disease - genetics; Coronary vessels; Gene expression; Genotype; Genotypes; Heart diseases; Humanities and Social Sciences; Humans; Leukocytes; Leukocytes - metabolism; multidisciplinary; Myocardial infarction; Myocardial Infarction - complications; Myocardial Infarction - genetics; Oxidation; Polymorphism, Genetic; Receptors, Immunologic - metabolism; Risk Factors; RNA, Messenger - genetics; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-22040-3

TREML4 and other members of the triggering receptor expressed in the myeloid cell family are associated with a risk of atherosclerosis and progression in coronary artery disease, acute coronary syndrome, and coronary artery calcification. Herein, the relationship between TREML4 expression and its polymorphisms (rs2803495 and rs280396) was evaluated in patients with subclinical atherosclerosis (n = 340) and heart failure post-acute myocardial infarction (MI) (n = 68) for the first time. TREML4 variants rs2803495 (A > G) and rs2803496 (T > C) and leukocyte mRNA expression was analyzed by qRT–PCR. The rs2803495 G allele was associated with TREML4 expression (OR 8.01, CI 3.78–16.99, p  < 0.001). Patients carrying the rs2803496 C minor allele (TC/CC genotypes) were more likely to express TREML4 than those without the C allele (OR 10.42, CI 4.76–22.78, p  < 0.001), as well as having higher levels of TREML4 expression (OR 4.88, CI 2.35–10.12, p  < 0.001). Thus, we report for the first time that TREML4 is not associated with the early stages of atherosclerotic plaque formation and later stages after MI. In conclusion, TREML4 mRNA expression in blood leukocytes is influenced by minor alleles (G and C) and may regulate differently during the atherosclerosis progression stages, but not in asymptomatic atherosclerosis disease and post-MI.