Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress.

Dysregulation of microRNA‑3613‑3p (miR‑3613‑3p) was previously reported in endothelial cells (ECs) during heat stress. The aim of the present study was to investigate the precise role of miR‑3613‑3p in heat stress. In the present study, potential gene targets of miR‑3613‑3p in heat‑treated ECs were assessed, and the potential effects of miR‑3613‑3p were determined using Gene Ontology enrichment analysis. Kyoto Encyclopedia of Genes and Genomes pathway analysis was used to identify signaling pathways that may be affected by miR‑3613‑3p in heat‑treated cells. Reverse transcription‑quantitative PCR, western blotting and annexin V‑FITC/propidium iodide staining were performed to detect miRNA expression, protein expression and apoptosis, respectively. Luciferase gene reporter assay was performed to evaluate the association between miR‑3613‑3p and mitogen‑activated protein kinase kinase kinase 2 (MAP3K2). Bioinformatics analysis revealed 865 potential gene targets for miR‑3613‑3p and a series of functions and pathways in heat‑treated ECs. 'Negative regulation of apoptotic process' was identified as a potential function of miR‑3613‑3p. In addition, functional analysis confirmed the downregulated expression levels of miR‑3613‑3p in ECs during heat stress, which was accompanied by an increase in apoptosis; restoration of miR‑3613‑3p expression inhibited apoptosis. MAP3K2 protein was demonstrated to be upregulated in heat‑treated ECs, and overexpression of miR‑3613‑3p reduced MAP3K2 expression levels. Additionally, MAP3K2 was targeted by miR‑3613‑3p. These results indicated that miR‑3613‑3p may have complicated roles in ECs under heat stress. miR‑3613‑3p may serve an important role in the apoptosis of heat‑treated ECs, and this effect may be partly achieved by targeting MAP3K2.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}