Hsa_circRNA_102541 regulates the development of atherosclerosis by targeting miR-296-5p/PLK1 pathway

Du, Na; Li, Mingjin; Yang, Dan

doi:10.1007/s11845-021-02708-x

Cited by 17 publications

(10 citation statements)

References 25 publications

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“…22) An investigation has documented that circ_102541 positively altered the PLK1 expression level through the mediation of miR-296-5p and thereby affected AS cell proliferation and apoptosis. 31) In this trial, we found that RFX7 was lowly expressed in ox-LDL-treated HUVECs, indicating that RFX7 might be involved in the progression of AS. RFX7 knockdown attenuated the protective effect of miR-616-3p downregulation on ox-LDL-induced injury, uncovering that miR-616-3p might promote AS progression by targeting RFX7.…”

Section: Disclosurementioning

confidence: 63%

Hsa_circ_0030042 Ameliorates Oxidized Low-Density Lipoprotein-Induced Endothelial Cell Injury via the MiR-616-3p/RFX7 Axis

Song

et al. 2022

Int. Heart J.

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Atherosclerosis (AS) is a common etiology of cardiovascular disease. As an emerging functional biomarker, circular RNAs (circRNAs) are involved in various diseases, including cardiovascular disease. However, the mechanism of action of circ_0030042 in AS has not been reported.Human umbilical vein endothelial cells (HUVECs) stimulated by ox-LDL served as a cellular model of AS. Gene expression was detected using quantitative real-time polymerase chain reaction. The influence of circ_ 0030042 on cell viability, proliferation, and apoptosis was verified using Cell Counting Kit-8, 5-ethynyl-2'deoxyuridine, and flow cytometry assays. An enzyme-linked immunosorbent assay was performed to measure the contents of tumor necrosis factor-α, interleukin (IL)-6, and IL-1β. Western blot assay was utilized to determine the protein levels of Bax, Bcl-2, PCNA, and regulatory factor X 7 (RFX7). The interrelationship between miR-616-3p and circ_0030042 or RFX7 was validated using dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays.The expression of circ_0030042 was downregulated in ox-LDL-induced HUVECs. It was found that overexpression of circ_0030042 facilitated cell proliferation, repressed apoptosis, and reduced the level of inflammatory factors in HUVECs. Circ_0030042 and miR-616-3p had a targeting relationship, and the miR-616-3p mimic eliminated the effects of overexpressed circ_0030042 on ox-LDL-induced HUVECs. RFX7 was a downstream gene of miR-616-3p and was lowly expressed in ox-LDL-induced HUVECs. The miR-616-3p inhibitor stimulated cell proliferation, arrested apoptosis, and caused a decline in the levels of inflammatory factors, whereas knockdown of RFX7 abolished the effects.Circ_0030042 weakened ox-LDL-induced HUVEC injury by regulating the miR-616-3p/RFX7 pathway, thereby influencing AS progression. Circ_0030042 is likely to be a potential biomarker for the future treatment of patients with AS.

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Section: Disclosurementioning

confidence: 63%

Hsa_circ_0030042 Ameliorates Oxidized Low-Density Lipoprotein-Induced Endothelial Cell Injury via the MiR-616-3p/RFX7 Axis

Song

et al. 2022

Int. Heart J.

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“…HtrA serine peptidase 2 ( HTRA2 ) and chromosome 9 open reading frame 64 ( C9orf64 ) have not been implicated in atherogenesis. Limited evidence indicates that polo like kinase 1 ( PLK1 ), encoding a stimulator of cell proliferation, and acyl-CoA oxidase 1 ( ACOX1 ), encoding a player in fatty acid metabolism, are upregulated in peripheral blood cells of atherosclerotic patients and linked to resolution of inflammation, respectively [ 19 , 20 ]. Furthermore, less than 10% of Horvath clock CpG were correlated with chronological age or histological grade (30 and 14, respectively) at nominal significance level (overall lowest significance p = 4.7x10 -4 ), but none reached genome-wide significance (p<10 −7 ;) ( S2 Table , S1 Fig ).…”

Section: Resultsmentioning

confidence: 99%

Dynamic epigenetic age mosaicism in the human atherosclerotic artery

Zaina

Esteller²,

Gonçalves³

et al. 2022

PLoS ONE

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Accelerated epigenetic ageing, a promising marker of disease risk, has been detected in peripheral blood cells of atherosclerotic patients, but evidence in the vascular wall is lacking. Understanding the trends of epigenetic ageing in the atheroma may provide insights into mechanisms of atherogenesis or identify targets for molecular therapy. We surveyed DNA methylation age in two human artery samples: a set of donor-matched, paired atherosclerotic and healthy aortic portions, and a set of carotid artery atheromas. The well-characterized pan-tissue Horvath epigenetic clock was used, together with the Weidner whole-blood-specific clock as validation. For the first time, we document dynamic DNA methylation age mosaicism of the vascular wall that is atherosclerosis-related, switches from acceleration to deceleration with chronological ageing, and is consistent in human aorta and carotid atheroma. At CpG level, the Horvath epigenetic clock showed modest differential methylation between atherosclerotic and healthy aortic portions, weak association with atheroma histological grade and no clear evidence for participation in atherosclerosis-related cellular pathways. Our data suggest caution when assigning a unidirectional DNA methylation age change to the atherosclerotic arterial wall. Also, the results support previous conclusions that epigenetic ageing reflects non-disease-specific cellular alterations.

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“…Reportedly, circRNAs can sponge miRNA to regulate the biological behavior of cells [ 25 ]. Additionally, the circRNA-miRNA-mRNA axis has been widely reported to interfere with the pathogenesis of AS [ 26 , 27 ]. To elucidate the regulating mechanism of circ_0026218 in ox-LDL-stimulated injury of HUVECs, we predicted the target miRNAs of circ_0026218 by bioinformatics analysis and discovered that miR-338-3p could be decoyed by circ_0026218.…”

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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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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Hsa_circRNA_102541 regulates the development of atherosclerosis by targeting miR-296-5p/PLK1 pathway

Cited by 17 publications

References 25 publications

Hsa_circ_0030042 Ameliorates Oxidized Low-Density Lipoprotein-Induced Endothelial Cell Injury via the MiR-616-3p/RFX7 Axis

Hsa_circ_0030042 Ameliorates Oxidized Low-Density Lipoprotein-Induced Endothelial Cell Injury via the MiR-616-3p/RFX7 Axis

Dynamic epigenetic age mosaicism in the human atherosclerotic artery

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

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