miR-92a-3p promotes ox-LDL induced-apoptosis in HUVECs via targeting SIRT6 and activating MAPK signaling pathway

Xu, Yingchun; Miao, Chunbo; Cui, Jinzhen; Bian, Xiaoli

doi:10.1590/1414-431x20209386

Cited by 16 publications

(6 citation statements)

References 35 publications

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“…SIRT6 reduces the generation of foam cells by prompting autophagy and cholesterol efflux under ox-LDL condition [ 35 ]. This study found that SIRT6 was lowly expressed in HUVECs with ox-LDL, which was coherent to the preceding study [ 23 ]. In addition, SIRT6 could be a downstream target of miR-338-3p in HUVECs.…”

Section: Discussionsupporting

confidence: 92%

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Circular RNA circ_0026218 Suppressed Atherosclerosis Progression via miR‐338‐3p/SIRT6 Axis

Yang¹,

Chen²,

Li³

et al. 2023

BioMed Research International

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Background. Multiple circular RNAs (circRNAs) are implicated in atherosclerosis (AS) pathogenesis. In fact, how circRNA 0026218 (circ_0026218) functions in AS remains unknown, and thus the functions and mechanisms of circ_0026218 in the injury of vascular endothelial cells are to be investigated. Methods. Microarray analysis was employed to screen out differentially expressed circRNAs in AS. A cell model was mimicked by treating Human umbilical vein endothelial cells (HUVECs) with oxidized low-density lipoprotein (ox-LDL). circ_0026218, microRNA-338-3p (miR-338-3p) and silent information regulator 6 (SIRT6) expressions in HUVECs with ox-LDL treatment were probed by qRT-PCR. The cell proliferative capabilities were exposed by CCK-8 assay. The contents of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor α (TNF-α) were measured by ELISA. Oxidative stress kits were utilized to detect the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA). Flow cytometry was adopted to analyze the level of apoptosis of HUVECs. Dual-luciferase reporter gene assay and RIP assay were leveraged to expose the interplay between miR-338-3p and circ_0026218 or SIRT6 3 ′ -UTR, respectively. In addition, the impacts of circ_0026216 and miR-338-3p on SIRT6 protein expressions were subjected to Western blot. Results. circ_0026218 was greatly depleted in ox-LDL-stimulated HUVECs. circ_0026218 overexpression promoted viability of HUVECs in vitro and inhibited inflammatory response, oxidative stress, and apoptosis. circ_0026218 could adsorb miR-338-3p and positively modulated SIRT6 expressions via sponging miR-338-3p. Upregulation of this miRNA reversed the influence of circ_0026218 overexpression on ox-LDL-caused injury and apoptosis of HUVECs. Conclusion. Collectively, circ_0026218 upregulates SIRT6 expression through decoying miR-338-3p, thereby inhibiting ox-LDL-initiated injury of HUVECs. circ_0026218 is involved in the pathogenesis of AS.

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Section: Discussionsupporting

confidence: 92%

“…Some studies have also covered vital roles of miRNAs in modulating the injury of vascular endothelial cells. For instance, miR-92a-3p accelerates ox-LDL-induced apoptosis of HUVECs via modulating the SIRT6/MAPK signaling pathway [ 23 ]. MiR-126-5p strengthens endothelial viability and limits AS via depressing DLK1 [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Circular RNA circ_0026218 Suppressed Atherosclerosis Progression via miR‐338‐3p/SIRT6 Axis

Yang¹,

Chen²,

Li³

et al. 2023

BioMed Research International

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“…The effect of let-7b-5p on the functioning of vascular smooth muscle cells is rarely reported. MiR-92a-3p promotes apoptosis of endothelial cells by targeting SIRT6 and activating MAPK signaling pathway ( 41 ). However, separate studies show that inhibition of miR-92a-3p regulates the development of atherosclerotic plaques ( 42 , 43 ).…”

Section: Discussionmentioning

confidence: 99%

Different Effects of Endothelial Extracellular Vesicles and LPS-Induced Endothelial Extracellular Vesicles on Vascular Smooth Muscle Cells: Role of Curcumin and Its Derivatives

Xiang

Cao

et al. 2021

Front. Cardiovasc. Med.

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Background: During the progression of atherosclerosis (AS), the vascular endothelial and smooth muscle cells are reciprocally regulated by extracellular vesicles (EVs). EVs have different effects on pathological and physiological processes due to the different cargoes contained in EVs.Purpose: To study the effects of endothelial cells-derived EVs on normal and inflammatory conditions. To investigate the effects of curcumin and curcumin derivatives (Nicotinic-curcumin) on endothelial EVs.Methods: EVs were isolated from human umbilical vein endothelial cells (HUVECs) by ultracentrifugation. To examined the effect of normal and LPS-induced endothelial cells-derived EVs on the proliferation of human aortic smooth muscle cells (HASMCs), the CCK-8 assay was performed. Transwell and wound healing assays were conducted to assess cell migration. The effects of EVs on lipid accumulation following treatment with oxidized low-density lipoprotein (Ox-LDL) were evaluated with the oil red O staining assay and HPLC. The number of EVs was calculated using the nanoparticle tracking analysis (NTA) and BCA. The expression levels of Rab27a and Rab27b that regulate the EVs secretion were measured by Western blotting assay. The differential expression of miRNAs in endothelial EVs and LPS-induced endothelial EVs was analyzed using miRNA-Sequencing (miRNA-Seq) and RT-PCR.Results: Treatment with endothelial EVs reduced the proliferation and migration of HASMCs as well as lipid accumulation in HASMCs. However, treatment with LPS-induced endothelial EVs did not inhibit the migration of HASMCs or lipid accumulation, instead it promoted the proliferation of HASMCs. Treatment with the two types of EVs induced differential expression of several miRNAs, including miR-92a-3p, miR-126-5p, miR-125a-3p, miR-143-3p, etc. Moreover, 1 μg/mL LPS induction greatly increased secretion of endothelial EVs. Treatment with curcumin and nicotinic-curcumin reduced endothelial EVs secretion, possibly by inhibiting inflammation.Conclusion: Endothelial EVs may confer beneficial effects on atherosclerosis by regulating vascular smooth muscle cell (VSMCs), whereas pro-inflammatory factors may disrupt this effect.

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“…Increasing evidence demonstrates that excessive oxidative stress can induce cell apoptosis and excessive apoptosis of vascular endothelial cells can destroy cardiovascular homeostasis, finally causing endothelial dysfunction and promoting the development of atherosclerosis [20] .…”

Section: Resultsmentioning

confidence: 99%

Harpagide Increases microRNA-140-5p Expression to inhibit Oxidised Low-Density Lipoprotein-Caused Human Umbilical Vascular Endothelial Cell Damage

Huang,

Zhao,

Huang

et al. 2023

IJPS

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To investigate the influence of harpagide isolated from Scrophularia ningpoensis Hemsl. on human umbilical vascular endothelial cells damage induced by oxidized low-density lipoprotein and its possible mechanism. Human umbilical vascular endothelial cells were cultured in vitro. Different doses (20, 40, 80 μmol/l) of harpagide were applied to treat human umbilical vascular endothelial cells induced by oxidized low-density lipoprotein, human umbilical vascular endothelial cells overexpressing microRNA-140-5p were induced by oxidized low-density lipoprotein, and 80 μg/ml harpagide was applied to treat oxidized low-density lipoprotein induced human umbilical vascular endothelial cells with microRNA-140-5p downregulation. Enzyme-linked immunosorbent assay kits were used to detect malondialdehyde content as well as superoxide dismutase and glutathione peroxidase activities. Flow cytometry and Western blot were utilized to investigate cell apoptosis. Ribonucleic acid expression was analyzed by real-time quantitative reverse transcription polymerase chain reaction. Different doses of harpagide (20, 40, 80 μmol/l) reduced the malondialdehyde content and the rate of apoptosis in oxidized low-density lipoprotein-stimulated human umbilical vascular endothelial cells (p<0.05), while elevated superoxide dismutase as well as glutathione peroxidase activities (p<0.05). MicroRNA-140-5p overexpression reduced the malondialdehyde content and apoptosis in oxidized low-density lipoproteinstimulated human umbilical vascular endothelial cells while elevated superoxide dismutase as well as glutathione peroxidase activities (p<0.05). Harpagide promoted microRNA-140-5p expression in human umbilical vascular endothelial cells after oxidized low-density lipoprotein stimulation (p<0.05). MicroRNA-140-5p knockdown reversed the inhibitory effect of harpagide in human umbilical vascular endothelial cells (p<0.05). Harpagide up-regulates microRNA-140-5p to inhibit the oxidative stress and apoptosis of oxidized low-density lipoprotein-induced human umbilical vascular endothelial cells.

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miR-92a-3p promotes ox-LDL induced-apoptosis in HUVECs via targeting SIRT6 and activating MAPK signaling pathway

Cited by 16 publications

References 35 publications

Circular RNA circ_0026218 Suppressed Atherosclerosis Progression via miR‐338‐3p/SIRT6 Axis

Circular RNA circ_0026218 Suppressed Atherosclerosis Progression via miR‐338‐3p/SIRT6 Axis

Different Effects of Endothelial Extracellular Vesicles and LPS-Induced Endothelial Extracellular Vesicles on Vascular Smooth Muscle Cells: Role of Curcumin and Its Derivatives

Harpagide Increases microRNA-140-5p Expression to inhibit Oxidised Low-Density Lipoprotein-Caused Human Umbilical Vascular Endothelial Cell Damage

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