Circulating miRNAs: novel biomarkers of acute coronary syndrome?

Acute coronary syndrome refers to any group of clinical symptoms compatible with acute myocardial infarction (AMI). AMI is a major cause of death and disability worldwide with the greatest risk of death within the first hours of AMI onset. Therefore, delays in 'ruling in' AMI may increase morbidity and mortality due to the time lag in initiating therapy. Likewise, since the majority of patients presenting with acute chest pain do not have AMI, the rapid 'ruling out' of AMI in those patients would increase emergency department triage efficiency, decrease medical costs, and reduce morbidity and mortality. Thus, the identification of novel biomarkers that improve current strategies and/or accurately identify subjects who are at risk of developing acute and chronic manifestations of cardiovascular disease are desperately needed. This article discusses the potential of peripheral blood microRNAs as clinical biomarkers for the diagnosis and prognosis of cardiovascular diseases such as AMI.

Regulation of the MIR155 host gene in physiological and pathological processes.

MicroRNAs (miRNAs), a family of small nonprotein-coding RNAs, play a critical role in posttranscriptional gene regulation by acting as adaptors for the miRNA-induced silencing complex to inhibit gene expression by targeting mRNAs for translational repression and/or cleavage. miR-155-5p and miR-155-3p are processed from the B-cell Integration Cluster (BIC) gene (now designated, MIR155 host gene or MIR155HG). MiR-155-5p is highly expressed in both activated B- and T-cells and in monocytes/macrophages. MiR-155-5p is one of the best characterized miRNAs and recent data indicate that miR-155-5p plays a critical role in various physiological and pathological processes such as hematopoietic lineage differentiation, immunity, inflammation, viral infections, cancer, cardiovascular disease, and Down syndrome. In this review we summarize the mechanisms by which MIR155HG expression can be regulated. Given that the pathologies mediated by miR-155-5p result from the over-expression of this miRNA it may be possible to therapeutically attenuate miR-155-5p levels in the treatment of several pathological processes.