Overexpression of microRNA‑506‑3p aggravates the injury of vascular endothelial cells in patients with hypertension by downregulating Beclin1 expression

Abstract

The aim of the present study was to measure the expression of microRNA (miRNA)-506-3p in the peripheral blood of patients with hypertension and to determine the biological functions and mechanisms of action of miR-506-3p. A total of 61 patients with primary hypertension were included in the present study. Peripheral blood was collected from all patients, as well as 31 healthy subjects who were included in a control group. The expression of miR-506-3p in peripheral blood was determined by reverse transcription-quantitative polymerase chain reaction. Human umbilical vein endothelial cells (HUVECs) were transfected with miR-506-3p mimics or miR-506-3p inhibitor. The proliferation and migration of HUVECs were determined using cell-counting kit 8 and Transwell assays, respectively. The cell cycle and apoptosis of HUVECs were detected by flow cytometry. The expression of Beclin1 (BECN1) protein, a potential target of miR-506-3p, was measured using western blotting. A dual-luciferase reporter assay was performed to determine the interaction between BECN1 and miR-506-3p. It was demonstrated that miR-506-3p expression in the peripheral blood of patients with patients was upregulated and dependent on the severity of hypertension. miR-506-3p overexpression inhibited the proliferation and migration of HUVECs. In addition, miR-506-3p inhibited the transition from the G1 phase to the S-phase in HUVECs. Overexpression of miR-506-3p promoted the apoptosis of HUVECs. Notably, miR-506-3p downregulated the expression of BECN1 by directly binding to its 3′-untranslated region. The present study demonstrated that miR-506-3p expression is elevated in the peripheral blood of patients with hypertension and is associated with the severity of hypertension. By downregulating BECN1 expression, miR-506-3p aggravates injury in vascular endothelial cells by inhibiting the proliferation and migration of HUVECs, as well as promoting their apoptosis.

MicroRNA-506 Is Involved in Regulation of the Occurrence of Lipopolysaccharides (LPS)-Induced Pulpitis by Sirtuin 1 (SIRT1)

“…It has been confirmed that miRNA quantity is a biomarker of specific diseases [18,19]. Previous studies showed that miR-506 may be involved in many activities, such as inflammation [13], cardiomyocyte dysfunction [20], malignant tumor development [21][22][23][24][25], stem cell differentiation [26], and epithelialmesenchymal transition [27], and have effects on primary biliary cirrhosis [28], rheumatoid arthritis [29], and blood vessel regeneration [30]. Therefore, miR-506 is associated with various cell biological processes, and this is consistent with the results of the present study.…”

Early Programming of Adult Systemic Essential Hypertension

“…An aberrant profile expression of miRNAs has been linked to a series of diseases, including hypertension and miRNA expression in the circulation shows changes in hypertensive subjects. Among the circulating levels of miRNAs that have been found to be elevated in hypertensive patients, the following can be mentioned: miR-221 and miR-222 [158], miR-92a [159,160], miR-21 and miR-1 [161] miR-516b, miR-600, miR-605, miR-623, and let-7e [162] and miR-506-3p [163]. Among the miRNAs that have been reported to be reduced in hypertensive patients, there is miR-143, miR-145, miR-133 [161], miR-18b, miR-30d, miR-296-5p, miR-324-3p, miR-486-5p, miR-518b, miR-1236, and miR-1227 [162].…”

MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

“…The ATG system is required for the LC3 to conjugate to phosphotidylethanolamine (PE) phospholipids and to form LC3 II. LC3 II is important for the expansion of the membrane, where it plays a crucial role in cargo recognition via its interaction to [178,181] miR-199a Up [184,188] EC dysfunction [185] mTOR, ULK1 [178,180,182,185] miR-101 Up [186,188] EC dysfunction [187] mTOR [178,179] miR-451 Up [193] Cardiac hypertrophy [193] AMPK [193,195] miR-148b Up [194] Hyperglycemia-induced EC dysfunction [155] AMPK [192] miR-20a Up [143] Regulates EC migration, angiogenesis and senescence [203,211] ULK1, FIP200 [199,208] miR-20b Up [209] Promotes EC senescence [210,211] FIP200 [208] miR-106b Up [204] EC proliferation and atherosclerosis [205] ULK1 [199,201] miR-17-5p Up [206] ECs apoptosis and cardiac dysfunction [207] ULK1 [202] miR-506-3p Unknown -Aggravates injury in vascular EC [212] Beclin 1 [ [212] miR-216a Unknown -Controls ox-LDL induced autophagy [216] Beclin 1 [216] miR-129-5p Up…”