Circular RNA circ_0010283 regulates the viability and migration of oxidized low‑density lipoprotein‑induced vascular smooth muscle cells via an miR‑370‑3p/HMGB1 axis in atherosclerosis

Ding, Peng; Ding, Yi; Tian, Ye; Lei, Xiaochun

doi:10.3892/ijmm.2020.4703

Cited by 32 publications

(26 citation statements)

References 34 publications

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“…Among several AS progression-associated circRNAs, including circ_0004104 [ 10 ], circ_0001879 [ 10 ], circ_0001445 [ 22 ], circ_0001599 [ 23 ], circ_0010283 [ 24 ] and circ_0007478 [ 25 ], we selected circ_0004104 for further analysis because it was the most significantly upregulated by ox-LDL (100 μg/mL, 24 h) in HUVECs (Additional file 1 : Figure 1 and Fig. 1 a).…”

Section: Resultsmentioning

confidence: 99%

“…“MiRNA sponge” mechanism is an important way by which circRNAs function in human diseases [ 26 , 32 ]. For example, circ_0010283 accelerated cell viability and motility of ox-LDL-treated vascular smooth muscle cells by sponging miR-370-3p and up-regulating HMGB1 [ 24 ]. Circ-PRMT5 contributed to gastric cancer development through up-regulating MYC via sponging miR-145 and miR-1304 [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

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Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis

Zhang¹,

Wang²,

Shen³

2021

BMC Cardiovasc Disord

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Background Circular RNAs have shown important regulatory roles in cardiovascular diseases, containing atherosclerosis (AS). We intended to explore the role of circ_0004104 in AS using oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial cells and its associated mechanism. Methods Real-time quantitative polymerase chain reaction and Western blot assay were conducted to analyze RNA levels and protein levels, respectively. Cell viability, apoptosis, angiogenic ability and inflammatory response were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay, flow cytometry, capillary-like network formation assay and enzyme-linked immunosorbent assay, respectively. Cell oxidative stress was assessed using commercial kits. Dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA-pull down assay were performed to verify the intermolecular interaction. Results ox-LDL exposure up-regulated the level of circ_0004104 in HUVECs. ox-LDL exposure suppressed cell viability and angiogenic ability whereas promoted the apoptosis, inflammation and oxidative stress of HUVECs partly through up-regulating circ_0004104. MicroRNA-328-3p (miR-328-3p) was confirmed as a target of circ_0004104. MiR-328-3p interference largely reversed circ_0004104 silencing-mediated effects in HUVECs upon ox-LDL exposure. MiR-328-3p interacted with the 3′ untranslated region of tripartite motif 14, and circ_0004104 positively regulated TRIM14 expression by sponging miR-328-3p. TRIM14 overexpression largely overturned miR-328-3p accumulation-induced influences in HUVECs upon ox-LDL exposure. Conclusion Circ_0004104 knockdown attenuated ox-LDL-induced dysfunction in HUVECs via miR-328-3p-mediated regulation of TRIM14.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis

Zhang¹,

Wang²,

Shen³

2021

BMC Cardiovasc Disord

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“…In terms of mechanism, plentiful studies have manifested that circRNAs regulate various biological functions in AS via participating in competing endogenous RNA (ceRNA) network ( 28 ). For instance, circ_0010283 facilitated the growth and migration of ox-LDL-stimulated VMSCs through sponging miR-370-3p and elevating HMGB1 expression ( 29 ). Circ_0124644 aggravated endothelial injury triggered by ox-LDL stimulation in HUVECs via absorbing miR-149-5p to activate PAPP-A ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

circ_0003204 Regulates Cell Growth, Oxidative Stress, and Inflammation in ox-LDL-Induced Vascular Endothelial Cells via Regulating miR-942-5p/HDAC9 Axis

Wan

You

Luo

2021

Front. Cardiovasc. Med.

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Background: Atherosclerosis (AS) is a typical inflammatory vascular disease. Many reports corroborated that circular RNAs (circRNAs) is involved in AS progression. However, the potential function and possible mechanism of circ_0003204 in AS progression remain indistinct.Methods: Expression level analysis was performed using qRT-PCR and western blot. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8), flow cytometry, and western blot assays. The status of oxidative stress and inflammation was determined via commercial detection kits and ELISA assay, respectively. The binding relationship was verified via dual-luciferase reporter and RNA immunoprecipitation assays.Results: ox-LDL increased circ_0003204 and HDAC9 levels and decreased miR-942-5p level. Silencing of circ_0003204 enhanced cell viability and inhibited cell apoptosis, oxidative stress and inflammation in ox-LDL-disposed HUVECs. In addition, circ_0003204 targeted miR-942-5p to regulate ox-LDL-resulted HUVECs injury. Also, miR-942-5p affected ox-LDL-triggered HUVECs injury by targeting HDAC9. Furthermore, circ_0003204 elevated HDAC9 expression via decoying miR-942-5p.Conclusion: circ_0003204 aggravated ox-LDL-induced HUVECs damage via modulating miR-942-5p/HDAC9 pathway.

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“…As for the function, ox-LDL-induced VSMCs’ excessive proliferation, colony-formation ability, migration, and cell cycle progression were attenuated by blocking circ_UBR4. Moreover, the suppressive role of circUBR4 knockdown in ox-LDL-induced proliferation, migration, and invasion in VSMCs had been previously demonstrated [ 34 , 35 ]. Molecularly, expression of PCNA and MMP2 was also depressed by blocking circ_UBR4 [ 35 ]; furthermore, circ_UBR4 modulated ox-LDL-evoked dysfunction of VSMCs through serving as a ceRNA for miRNAs, such as miR-133a-3p and miR-370-3p.…”

Section: Discussionmentioning

confidence: 99%

Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle cells in atherosclerosis

Zhang

Chen

et al. 2021

Open Life Sciences

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The circ_UBR4 (hsa_circ_0010283) is a novel abnormally overexpressed circRNA in oxidized low-density lipoprotein (ox-LDL)-induced model of atherosclerosis (AS) in human vascular smooth muscle cells (VSMCs). However, its role in the dysfunction of VSMCs remains to be further investigated. Here, we attempted to explore its role in ox-LDL-induced excessive proliferation and migration in VSMCs by regulating Rho/Rho-associated coiled-coil containing kinase 1 (ROCK1), a therapeutic target of AS. Expression of circ_UBR4 and ROCK1 was upregulated, whereas miR-107 was downregulated in human AS serum and ox-LDL-induced VSMCs. Depletion of circ_UBR4 arrested cell cycle, suppressed cell viability, colony-forming ability, and migration ability, and depressed expression of proliferating cell nuclear antigen and matrix metalloproteinase 2 in VSMCs in spite of the opposite effects of ox-LDL. Notably, ROCK1 upregulation mediated by plasmid transfection or miR-107 deletion could counteract the suppressive role of circ_UBR4 knockdown in ox-LDL-induced VSMCs proliferation, migration, and cell cycle progression. In mechanism, miR-107 was identified as a target of circ_UBR4 to mediate the regulatory effect of circ_UBR4 on ROCK1. circ_UBR4 might be a contributor in human AS partially by regulating VSMCs’ cell proliferation, migration, and cell cycle progression via circ_UBR4/miR-107/ROCK1 pathway.

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Circular RNA circ_0010283 regulates the viability and migration of oxidized low‑density lipoprotein‑induced vascular smooth muscle cells via an miR‑370‑3p/HMGB1 axis in atherosclerosis

Cited by 32 publications

References 34 publications

Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis

Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis

circ_0003204 Regulates Cell Growth, Oxidative Stress, and Inflammation in ox-LDL-Induced Vascular Endothelial Cells via Regulating miR-942-5p/HDAC9 Axis

Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle cells in atherosclerosis

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