MicroRNAs (miRNAs) are a group of endogenous noncoding small RNAs characterized by high conservation; furthermore, various studies have shown the capability of miRNAs to impact diseases. For example, a study shows that cellfree miRNAs are stable in bodily fluids, which gives circulating miRNAs the ability to be potential biomarkers for noninvasive diagnosis. Additionally, accumulating studies have supported that miRNAs can function as suppressor genes, again demonstrating their effect on disease. This review introduces this particular role of miRNAs as well as analyzes the prospect of miRNAs as biomarkers and the capacity for using miRNA-based resources to benefit mankind.

Background The mechanism underlying burn injury-induced enhanced vascular endothelial permeability and consequent body fluid extravasation is unclear. Here, the rat aortic endothelial cells (RAECs) were treated with the serum derived from rats with burn injury to elucidate the mechanism Methods Sprague-Dawley (SD) rats were grouped as follows (10 rats/group): control, 2, 4, 8, 12, and 24 h post-burn groups. The heart, liver, kidney, lung, jejunum, and ileum of rats injected with 2% Evans blue (EB) through the tail vein were excised to detect the EB level in each organ. The serum levels of hypoxia-inducible factor-1α (HIF-1α) and endothelin-1 (ET-1) were examined using enzyme-linked immunosorbent assay (ELISA). The effect of serum from 12 h post-burn group on the membrane permeability of RAEC monolayer, as well as on the mRNA and protein levels of ET-1, endothelin receptor A (ETA), ETB, and zonula occludens (ZO-1), were analyzed using quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The membrane permeability of GV230/HIF-1α-transfected or shRNA-HIF-1α-transfected RAECs, as well as the expression levels of HIF-1α, ET-1, ETA, ETB, vascular endothelial (VE)-cadherin, and claudin-5, were analyzed using qRT-PCR and western blotting, while the localization of VE-cadherin and claudin-5 was examined using immunofluorescence Results The serum HIF-1α and ET-1 levels in the burn groups, which peaked at 12 h post-burn, were significantly upregulated (P<0.01) when compared with those in the control group. Additionally, the serum HIF-1α levels were positively correlated with vascular permeability. Compared with the shRNA-negative control-transfected RAECs, the shRNA-II/HIF-1α-transfected RAECs exhibited downregulated expression of HIF-1α, ET-1, ETA, and ETB (P<0.01), and upregulated expression of ZO-1, claudin-5, and VE-cadherin (P<0.05). Compared with the GV230-transfected RAECs, the GV230/HIF-1α-transfected RAECs exhibited upregulated expression of HIF-1α, ET-1, ETA, and ETB (P<0.01), and downregulated expression of ZO-1, claudin-5, and VE-cadherin (P<0.05). The GV230/HIF-1α-transfected RAECs exhibited degradation and translocation of VE-cadherin and claudin-5 Conclusion In addition to degradation of VE-cadherin and claudin-5, HIF-1α mediated enhanced endothelial cell permeability through upregulation of ET-1, ETA, and ETB, and downregulation of ZO-1 and VE-cadherin in rats with burn injury

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