Identification of microRNAs as potential cellular monocytic biomarkers in the early phase of myocardial infarction: a pilot study

Abstract

MicroRNA has been increasingly suggested to be involved in vascular inflammation. The aim of this study was to assess the expression profile of miRs as possible novel cellular biomarkers in circulating monocytes in patients with ST-segment elevation myocardial infarction (STEMI). Microarray techniques and TaqMan polymerase chain reaction were used to analyse the global expression of 352 miRNAs in peripheral blood monocytes from healthy donors (n = 20) and patients (n = 24) with acute STEMI. The expression level of miR-143 in monocytes from STEMI patients compared to healthy controls was increased, whereas the expression of miR-1, -92a, -99a, and -223 was reduced significantly. During 3.5 ± 1.5 months of follow-up miR-1 and -223 were back to baseline, whereas miR-92a and -99a return to normal levels over 3 months, but remained lower than healthy controls. Furthermore, monocytic expression of miR-143 was positively correlated with hs-CRP (R2 = 0.338; P < 0.031), but not with cTnT. Importantly, treatment of monocytes isolated from healthy individuals with INFγ, but not LPS or TNFα caused an upregulation of miR-143 and downregulation of miR-1. Our findings identify circulating monocytes as putative biomarkers and as novel carriers for the cell-specific transfer of miRs in the early phase of myocardial infarction.

Role of miRNAs induced by oxidized low-density lipoproteins in coronary artery disease: the REGICOR Study

“…In accordance to our results, the 12 overexpressed miRNAs in the case-control study, were identified as significantly upregulated in individuals with AMI or CAD in previous studies [45,[49][50][51][52], or after cardiac ischaemia in animal models (miR-15 family) [53].…”

“…These miRNAs have been associated with 1) apoptosis in ECs and cardiomyocytes (has-miR-16-5p, has-miR-499a-5p, has-miR-21-5p, has-miR-22-3p, and has-miR-125b-5p) [54][55][56][57]; 2) proliferation and differentiation in VSMCs and cardiomyocytes (has-miR-145-5p, has-miR-143-3p, and has-miR-133a-3p) [49,58,59]; 3) angiogenesis (has-miR-222-3p, and has-miR-22-3p) [58]; 4) secretion of pro-inflammatory cytokines (has-miR-186-5p, All rights reserved. No reuse allowed without permission.…”

Expression profiling and bioinformatics analysis of circulating microRNAs in patients with acute myocardial infarction

“…11 And study identified circulating monocytes as novel biomarkers and carriers for the cell-specific transfer of miRNAs in the early stage of myocardial infarction. 39 Some findings strengthen the potential of applying miRNAs, such as miR-708, to reconstitute lost cardiomyocytes in injured hearts and may provide a novel candidate for promoting heart regeneration. 40 Therefore, with further improving the miRNA detection technology, miRNA may become a marker for early diagnosis and treatment of AMI.…”

“…A study has revealed an important role of miRNAs as biomarkers of AMI and its associated symptoms, and their role in disease diagnosis, platelet activation monitoring, and prognostic outcome prediction . And study identified circulating monocytes as novel biomarkers and carriers for the cell‐specific transfer of miRNAs in the early stage of myocardial infarction . Some findings strengthen the potential of applying miRNAs, such as miR‐708, to reconstitute lost cardiomyocytes in injured hearts and may provide a novel candidate for promoting heart regeneration .…”

Noncoding RNAs as Biomarkers for Acute Coronary Syndrome

“…In addition, the expression level of mir-1 in peripheral blood of ACS patients was higher than that of non-ACS patients, and the expression level of miR-1 in UA patients was significantly higher than that of NSTEMI [15]. Although the expression level of miR-1 in the peripheral blood plasma or serum of AMI patients was increased, the expression level of miR-1 in the circulating monocytes of STEMI patients was significantly decreased [16]. The reason for this difference may be due to the cellular source of miR-1.…”