Elevated miR‑195‑5p expression in deep vein thrombosis and mechanism of action in the regulation of vascular endothelial cell physiology
- Jinlong Jin
- Caixia Wang
- Yujuan Ouyang
- Dandan Zhang
Affiliations: Interventional Department of Peripheral Vascular Disease, Gansu Provincial Hospital of TCM, Lanzhou, Gansu 730050, P.R. China, Department of Basic Nursing, Health School of Nuclear Industry, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, P.R. China, Institute of Clinical Research, Communicable Diseases Department, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, P.R. China
- Published online on: November 4, 2019 https://doi.org/10.3892/etm.2019.8166
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Deep vein thrombosis (DVT) is one of the most common cardiovascular diseases. The apoptosis of vascular endothelial cells is the most important cause of venous thrombosis. MicroRNAs (miRNAs) play important roles in the regulation of cell apoptosis. miRNA (miR)‑195 is upregulated in the blood of patients with DVT, and it was predicted that Bcl‑2 is a potential target of miR‑195‑5p. Therefore, it was hypothesized that miR‑195‑5p may play an important role in the development of DVT by targeting Bcl‑2. The present study aimed to investigate the expression of miR‑195‑5p in DVT patients, and to explore whether miR‑195‑5p is involved in the development of DVT by regulating the apoptosis of vascular endothelial cells. The level of miR‑195‑5p was detected using reverse transcription‑quantitative PCR. Dual luciferase reporter assays were used to determine the relationship between Bcl‑2 and miR‑195‑5p. Cell viability was detected using MTT assays, and cell apoptosis was analyzed by flow cytometry. Protein levels of Bcl‑2 and Bax were measured by western blotting. The results indicated that miR‑195‑5p was significantly upregulated in the blood of DVT patients. It was also revealed that Bcl‑2 was a direct target of miR‑195‑5p, and that Bcl‑2 was downregulated in the blood of patients with DVT. miR‑195‑5p downregulation promoted cell viability and inhibited the apoptosis of human umbilical vein endothelial cells (HUVECs). miR‑195‑5p upregulation inhibited cell viability and increased the apoptosis of HUVECs. All of the observed effects of miR‑195‑5p upregulation on HUVECs were reversed by raised Bcl‑2 expression. In conclusion, miR‑195‑5p was significantly upregulated in patients with DVT, and it may be involved in the development of DVT by regulating the apoptosis of vascular endothelial cells. Therefore, miR‑195‑5p may be a potential target for predicting and treating DVT.