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• Present study comprehends significant role of MicroRNAs in VTE pathogenesis. • Review highlights the strengths and weaknesses of MiRNAs as biomarkers and therapeutic targets. • This review could make the way for future research and exploration in this area. Venous Thrombo-embolism (VTE) is the major preventable cause of death and disability worldwide. It has the third highest incidence rate of hospital death after coronary artery disease (CAD) and stroke. With the establishment of Virchow's triad stating the major factors responsible for VTE including stasis, hypercoagulability and endothelial dysfunction, the last decade reported number of studies regarding its diagnosis and prophylaxis. Till date the most commonly used clinical marker for its diagnosis is the D-dimer test, detecting endogenous fibrinolysis. This test often gives false positive results and has low specificity. Other markers of coagulation are being used in combination with D-dimer; however, a reliable and sensitive biomarker is still needed for early and accurate diagnosis of VTE. Non-coding regulatory RNAs such as MicroRNAs (miRNAs) are small molecules that play a significant role in RNA silencing and post-transcriptional gene expression regulation. They can specifically bind to their target genes forming silencing complex, thereby inducing degradation and altered gene expression. A wide range of miRNAs have extensively been studied in a variety of cardiovascular diseases such as CAD, stroke, myocardial infarction (MI), atherosclerosis, obstructive sleep apnoea (OSA) and other complex diseases such as cancer. It has been demonstrated that circulating miRNAs have enormous potential to function as clinical diagnostic biomarkers for many diseases. This review comprehends recent studies establishing the inevitable role of miRNAs in pathogenesis of complex diseases with special emphasis on venous thrombosis. The differential expression pattern of these miRNAs shows a strong positive correlation with the manifestation of the pathological symptoms of diseases. Systematic consolidation of different miRNAs linked to VTE in various studies could be helpful in finding accurate diagnostic markers for thrombosis and may also find its place in VTE therapeutics. However, more extensive research and confirmatory experiments are needed to establish the role of these miRNAs as biomarkers. [ABSTRACT FROM AUTHOR]

Background Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world. The biology of this disease remains elusive. In the present times, targeted molecular therapy defines the treatment. This has made understanding the elusive biology and molecular mechanisms of the disease more relevant. MicroRNAs (miRNAs) are non-encoding RNAs that play important gene-regulatory roles in neoplastic processes. As in silico studies list nearly hundreds and more target genes for each miRNA, it is of interest to see if there are genes that have already been implicated in this disease. Objective The purpose of this study was to identify genes regulated by miRNAs that are independently implicated in the pathogenesis of CLL in previously published literature. Material and methods Eight miRNAs were selected. Genes implicated in the biology of CLL in association studies and massively parallel sequence studies were selected. TargetScanHuman 6.2, a computational program that predicts target genes of miRNAs on the basis of sequence analysis, was used to link the miRNAs to genes of interest. Results The genes targeted by miR-15a, miR-223, miR-29a, and miR181a included IL10RA, BCL2, BCL6, DDX3X, and FBXW7. The most significant link observed was that several gene members of the TNF/TNFR superfamily were targets of miR-15a, miR-29a, and miR-181a. Conclusion MiRNAs implicated in the pathogenesis of CLL regulate genes that have independently been shown to play a role in CLL. The link between miRNAs and the TNF/TNFR superfamily is especially exciting. Understanding the molecular basis of these links in future studies may pave the way for using these miRNAs as therapeutic targets in CLL. [ABSTRACT FROM AUTHOR]

Aims The number of Sertoli cells during proliferative phase determines the fate of the germ cells in male reproductive system. A well-characterized cell line may help in better understanding of Sertoli cell biology. Hence, the present study assessed estradiol signaling in a mouse immature Sertoli cell line (MSC-1) as an alternative model in place of primary culture of Sertoli cells. Main methods In this study, we used MSC-1 cell line, derived from 10-day old mice. The cell cycle parameters were assessed, and the expression and regulation of Sertoli cell-specific secretory genes ( ABP ; androgen-binding protein ) and tight junction genes ( claudin-5 , occludin , and vimentin ) in response to estradiol was studied. Key findings The results obtained suggested the presence of both estrogen receptors (ERα and ERβ) in MSC-1 cells. In vitro scratch assay and cell-cycle analysis suggested the proliferative effects of estradiol in both time- and dose-dependent manner. The gene expression profiles of ABP , claudin-5 , and occludin showed biphasic regulation at low and high doses of estradiol. Analysis of signaling pathways suggested the activation of extracellular signal-regulated kinase (ERK) pathway with significantly increased pERK/ERK ratio ( p < 0.05). The results also suggested down regulation in the expression of mir-17 family members (mir-17, mir-20b, and mir-106a) ( p < 0.05). Significance Considering the limited number of Sertoli cell lines and long-term survival inability of primary culture of Sertoli cells, MSC-1 cells could be a potential cell line for understanding the mechanisms of various cellular events in Sertoli cells. [ABSTRACT FROM AUTHOR]