MicroRNAs: Potential Biomarkers and Targets of Therapy in Allergic Diseases?

Abstract

MicroRNAs (miRNAs) are small non-coding RNA molecules that are 18–22 nucleotides long and highly conserved throughout evolution. Currently, they are considered one of the fundamental regulatory mechanisms of genes expression. It has been demonstrated that miRNAs are involved in many biologic processes, such as signal transduction, cell proliferation and differentiation, apoptosis and stress responses. More recently, the role of miRNA has also been revealed in numerous immunological and inflammatory disorders, including allergic inflammation. Specific miRNA profiles were demonstrated in asthma, allergic rhinitis and atopic dermatitis. A core set of miRNAs involved in atopic diseases include upregulated miR-21, miR-223, miR-146a, miR-142-5p, miR-142-3p, miR-146b, miR-155 and downregulated let-7 family, miR-193b and miR-375. Most of the involved miRNAs increase secretion of Th2 cytokines (miR-1248, miR-146b), decrease secretion of Th1 cytokines (miR-513-5p, miR-625-5p) or promote differentiation of T cells towards Th2 (miR-21, miR-19a). In asthma miR-140-3p, miR-708 and miR-142-3p play a role in hyperplasia and hypertrophy of bronchial smooth muscle cells. Some single miRNAs or, more probably, their sets hold the promise for their use as biomarkers of atopic diseases. They are also promising target of future therapies.

Head and neck squamous cancer progression is marked by CLIC4 attenuation in tumor epithelium and reciprocal stromal upregulation of miR-142-3p, a novel post-transcriptional regulator of CLIC4

“…Additional data support the use of miR-142-3p as a biomarker due to elevation of circulating miR-142-3p levels in various pathological states . In fact, a recent review defined miR-142-3p as one of a core set of biomarker miRNAs for atopic diseases because of its frequent association with allergic inflammation and immune cell dysfunction [97].…”

Belinostat resolves skin barrier defects in atopic dermatitis by targeting the dysregulated miR-335:SOX6 axis

“…[11][12][13] Altered miRNA expression in skin has been documented in systematic inflammatory diseases, including AD. 14 However, the bulk of existing miRNA studies are either correlative 15,16 or focus mainly on immune dysfunction. [17][18][19] Here, we investigate microRNAs that are critical to maintain skin barrier function, and we identify miR-335 as a key driver of keratinocyte differentiation and cornification.…”

The role of epigenetics in the development of childhood asthma

“…Noncoding RNA, such as microRNA (miRNA) is relevant in posttranscriptional control and regulation of pathological processes in disease. Many miRNAs have been identified to be associated with asthma in various tissues including blood cells, airway epithelial cells and smooth muscle, and some miRNAs are considered to be potential biomarkers and promising therapy targets for asthma [44,45]. As reviewed previously, some asthma-associated miRNAs may target genes related to immune function (such as miR-155, miR-210, miR-21, and miR-19a), and some may function on genes related to airway function (such as miR-140-3p, miR-708, and miR-10) [44].…”

“…Many miRNAs have been identified to be associated with asthma in various tissues including blood cells, airway epithelial cells and smooth muscle, and some miRNAs are considered to be potential biomarkers and promising therapy targets for asthma [44,45]. As reviewed previously, some asthma-associated miRNAs may target genes related to immune function (such as miR-155, miR-210, miR-21, and miR-19a), and some may function on genes related to airway function (such as miR-140-3p, miR-708, and miR-10) [44]. For example, a recent study of miRNA expression profiles in IL-22and IL-17-positive T cells sorted from human PBMCs showed higher expression levels of miR-323-3p in asthmatics and a reverse correlation between miR-323-3p levels and IL-22 production, suggesting a negative feedback mechanism of miR-323-3p that controls the production of IL-22 in IL-22/IL-17-producing T cells in asthma [46].…”