MicroRNAs (miRNAs) are a group of endogenous non-coding RNAs that regulate gene expression. Alteration in miRNA expression results in changes in the profile of genes involving a range of biological processes, contributing to numerous human disorders. With high stability in human fluids, miRNAs in the circulation are considered as promising biomarkers for diagnosis, as well as prognosis of disease. In addition, the translation of miRNA-based therapy from a research setting to clinical application has huge potential. The aim of the current review is to: (i) discuss how miRNAs traffic intracellularly and extracellularly; (ii) emphasize the role of circulating miRNAs as attractive potential biomarkers for diagnosis and prognosis; (iii) describe how circulating microRNA can be measured, emphasizing technical problems that may influence their relative levels; (iv) highlight some of the circulating miRNA panels available for clinical use; (v) discuss how miRNAs could be utilized as novel therapeutics, and finally (v) update those miRNA-based therapeutics clinical trials that could potentially lead to a breakthrough in the treatment of different human pathologies.

Long non-coding RNAs (lncRNAs) are non-coding RNA molecules longer than 200 nucleotides that regulate gene expression at the transcriptional, post-transcriptional, and translational levels. Abnormal expression of lncRNAs has been identified in many human diseases. Future improvements in diagnostic, prognostic, and therapeutic techniques will be facilitated by a deeper understanding of disease etiology. Cardiovascular diseases (CVDs) are the main cause of death globally. Cardiac development involves lncRNAs, and their abnormalities are linked to many CVDs. This review examines the relationship and function of lncRNA in a variety of CVDs, including atherosclerosis, myocardial infarction, myocardial hypertrophy, and heart failure. Therein, the potential utilization of lncRNAs in clinical diagnostic, prognostic, and therapeutic applications will also be discussed.

The miR-144-3p was discovered to upregulate in osteoarthritis. However, the function of this molecule is still poorly understood. Identification of microRNA target genes could shed a light on miRNA functions. In this project, we aim to identify a direct target of miR-144-3p. Potential targets of miR-144-3p were predicted by bioinformatic algorithms. Expression of ADAMTSL3 in miRNA-144-3p gain-and- loss- of function experiment was quantified by Realtime-PCR. Next, the 3’UTR of ADAMTSL3 containing miR-144-3p-binding sites was subcloned in the 3’;UTR of the Firefly luciferase gene on the pmiRGlo. To test the complementary binding of miR-144-3p to ADAMTSL3 mRNA, we employed the luciferase assay using pmiRGlo-ADAMTSL3 vector or pmiRGlo-ADAMTSL3 mutant in which miR-144-3p binding sites in the 3’UTR was mutated. Results showed that miRNA-144-3p directly inhibits the expression of ADAMTSL3 through its ability to pair at “seed” sites. This study provides evidence for the interaction of miRNA-144-3p and its target, ADAMTSL3 mRNA, in chondrocytes.

MiR-3085-3p was shown to play a crucial role in cartilage biology, with potential impacts in osteoarthritis (OA). Insight into this miRNA function could be of practical importance for future miRNA-based therapy, however, little is known regarding the biological roles of this miRNA. The physiologic function of an individual miRNA is dictated through its mRNA targets, and as SCIN (scinderin, also known as adseverin) was reported to be involved in chondrocyte differentiation, maturation, and phenotype maintenance, this study aimed to prove SCIN is a direct target of miRNA-3085-3p. Bioinformatics algorithms were utilized for predicting their interacting sites. Gain- and loss-of-function experiments with miRNA-3085-3p were performed and SCIN expression was measured by real-time RT-PCR. SCIN 3?UTR regions harboring either the miR-3085-3p seed site or its mutant version were cloned into pmirGLO downstream of a reporter firefly luciferase encoding gene. The effect of miR-3085-3p on this region was determined by the luciferase assay. Four binding sites of miR-3085-3p in SCIN 3?UTR were identified. SCIN expression level was found to be inversely correlated with the level of miRNA-3085-3p. MiR3085-3p directly binds to its binding sites in SCIN 3? UTR. These data suggest that SCIN is the direct target of miR-3085-3p in chondrocyte cells.