scholarly journals CircRNA RERE Promotes the Oxidative Stress-Induced Apoptosis and Autophagy of Nucleus Pulposus Cells through the miR-299-5p/Galectin-3 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Rong Wang ◽  
Xingchao Zhou ◽  
Guorui Luo ◽  
Jin Zhang ◽  
Min Yang ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Nucleus Pulposus ◽  
Molecular Mechanisms ◽  
Cell Loss ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Nucleus Pulposus Cells ◽  
Galectin 3 ◽  
Induced Apoptosis

Intervertebral disc degeneration (IDD) is widely accepted as a cause of low back pain and related degenerative musculoskeletal disorders. Nucleus pulposus (NP) cell loss is closely related to IDD progression. Thus, investigating the specifically targeted therapeutic agents against NP cell loss depends on understanding the molecular mechanisms. In this study, human NP cells were treated with hydrogen peroxide (H2O2). Cell viability was assessed by using the Cell Counting Kit-8 (CCK-8) kit. The expression of circRNA arginine-glutamic acid dipeptide repeats (hsa_circ_RERE) and miR-299-5p was analyzed by real-time quantitative PCR. Western blot analysis was used to assess the protein expression levels. The autophagy levels in NP cells were detected by using an electronic microscope, LC3B protein immunofluorescence, and western blot. The apoptosis levels of NP cells were detected by flow cytometry and western blot. Dual-luciferase reporter assay analyzed the miR-299-5p bound to circ_RERE and galectin-3. Our results revealed that H2O2 significantly inhibited the viability of NP cells, promoted apoptosis and autophagy, and upregulated galectin-3 expression. miR-299-5p was reduced in IDD and H2O2-induced NP cells. The overexpression of miR-299-5p promoted cell viability and attenuated apoptosis and autophagy under H2O2 treatment. Besides, circ_RERE was upregulated in IDD and H2O2-induced NP cells. However, knockdown of circ_RERE reversed the effects of miR-299-5p overexpression on cell viability, apoptosis, and autophagy in NP cells. We propose that circ_RERE promotes the H2O2-induced apoptosis and autophagy of NP cells through the miR-299-5p/galectin-3 axis and may provide a new target for the clinical treatment of IDD.

VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Aikebaier Maimaiti ◽  
Amier Aili ◽  
Hureshitanmu Kuerban ◽  
Xuejun Li
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Gallic Acid ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Dependent Manner ◽  
Lung Carcinoma Cells ◽  
Induced Apoptosis ◽  
The Impact

Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability.

scholarly journals Knockdown of Circ_SLC39A8 protects against the progression of osteoarthritis by regulating miR-591/IRAK3 axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jizhe Yu ◽  
Yushuang Qin ◽  
Naxin Zhou
Keyword(s):  
Cell Viability ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Oa Chondrocytes ◽  
Polymerase Chain ◽  
Apoptosis And Inflammation ◽  
The Relationship

Abstract Background The dysregulation of circular RNAs (circRNAs) has been identified in various human diseases, including osteoarthritis (OA). The purpose of this study was to identify the role and mechanism of circ_SLC39A8 in regulating the progression of OA. Methods The expression levels of circ_SLC39A8, miR-591, and its potential target gene, interleukin-1-receptor-associated kinase 3 (IRAK3), were identified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The relationship between miR-591 and circ_SLC39A8 or IRAK3 was predicted by bioinformatics tools and verified by dual-luciferase reporter. Results Circ_SLC39A8 and IRAK3 were upregulated and miR-591 was downregulated in OA cartilage tissues. Knockdown of circ_SLC39A8 inhibited apoptosis and inflammation in OA chondrocytes, while these effects were reversed by downregulating miR-591. Promotion cell viability effects of miR-591 were partially reversed by IRAK3 overexpression. Conclusion Our findings indicated that knockdown of circ_SLC39A8 delayed the progression of OA via modulating the miR-591-IRAK3 axis, providing new insight into the molecular mechanisms of OA pathogenesis.

scholarly journals Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Hao Jie Zhang ◽  
Xue Hai Ma ◽  
Song Lin Xie ◽  
Shu lian Qin ◽  
Cong Zhi Liu ◽  
...  
Keyword(s):  
Nucleus Pulposus ◽  
General Characteristic ◽  
Luciferase Reporter ◽  
Healthy Controls ◽  
Nucleus Pulposus Cells ◽  
Apoptosis Rate ◽  
Tnf Α ◽  
Significant Difference ◽  
Induced Apoptosis

Abstract Background Intervertebral disc degeneration (IVDD) is a well-known cause of lower back pain, which is induced by multiple factors including increased apoptosis and decreased survival of nucleus pulposus cells. In this study, we evaluate the effect and potential mechanism of miR-660 on the nucleus pulposus cells apoptosis induced by TNF-α. Methods First, we collected tissue of nucleus pulposus from IVDD and healthy controls. General characteristic of the IVDD and healthy control was also collected. And, we also collected nucleus pulposus cells that stimulated by TNF-α or control. miRNA microarray was performed to identify the differentially expressed miRNAs. Apoptosis rate and miR-660 relative expression was measured after stimulated with different concentration of TNF-α to identify the optimal concentration of TNF-α. Second, we successfully constructed antigomiR-660 to block the miR-660 expression in nucleus pulposus cells and then stimulated with TNF-α (100 ng/ml, 12 h). The apoptosis rates and relative protein expression were then measured again. The target association between miR-660 and SAA1 was confirmed by dual-luciferase reporter. Results There was no significant difference between the age (IVDD: 39 ± 10 years, healthy controls: 36 ± 7 years), BMI and sex between IVDD and healthy controls. Microarray analysis found that miR-660 was significantly up-regulated in IVDD and TNF-α treated groups, which was further identified by PCR. We found that the rate of apoptosis and miR-660 expression increased with TNF-α concentration increased. Finally, TNF-a with 100 ng/ml was used for further experiment. Compared with TNF-α group, TNF-α + antigomiR-660 could significantly down-regulated the apoptosis rate and relative protein (c-Caspase3 and c-Caspase7). Dual-luciferase reporter revealed that miR-660 could directly binding to the SAA1 at 80–87 sites. Compared with TNF-α alone group, TNF-α + antigomiR-660 significantly up-regulated the SAA1 expression (P < 0.05). Conclusion These results indicated that knockdown of miR-660 protected the nucleus pulposus from apoptosis that induced TNF-α via up-regulation of SAA1. Further studies should focus on the role of miR-660 in protecting IVDD in vivo.

scholarly journals Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy through inhibiting NF-κB activation

2020 ◽  
Author(s):  
Min Han ◽  
Xiao-Cui Chen ◽  
Ming-Hui Sun ◽  
Min-Tao Gai ◽  
Yi-Ning Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Western Blot ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Neonatal Rat ◽  
Cell Counting ◽  
Pyrrolidine Dithiocarbamate ◽  
Induced Apoptosis

Abstract Background: Inflammation and oxidative stress play a predominant role in the initiation and progression of ischemia/reperfusion (I/R) injury, of which nuclear factor kappa B (NF-κB) is a crucial mediator. Overexpression of the inhibitor of κB alpha (IκBα) gene is hypothesized to have protective effects against apoptosis and autophagy in cardiomyocytes subjected to hydrogen peroxide (H2O2) through inhibiting the NF-κB pathway.Methods: The IκBαS32A, S36A gene was transfected via adeno-associated virus serotype 9 (AAV9) delivery into neonatal rat ventricular cardiomyocytes (NRVMs) prior to H2O2 treatment. NRVMs were divided into control, H2O2, GFP +H2O2, IκBα+H2O2, and pyrrolidine dithiocarbamate (PDTC)+H2O2 groups. Nuclear translocation of NF-κB p65 subunit was evaluated by immunofluorescence and Western blot. Cell viability was assessed by Cell Counting Kit-8 assay. Supernatant lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA) were measured to identify H2O2-stimulated cytotoxicity. Apoptosis was determined by Annexin V-PE/7-AAD staining, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. Western blot was used to detect apoptosis- and autophagy-related proteins.Results: IκBα transfection significantly increased cell viability and ΔΨm, but decreased the supernatant LDH and cellular MDA levels in cardiomyocytes exposed to H2O2. Meanwhile, IκBα overexpression decreased H2O2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-Ⅱ/LC3-Ⅰ ratio. These effects partly accounted for the ability of IκBα to inhibit the NF-κB signaling pathway, as evidenced by decreases in p65 phosphorylation and nuclear translocation. Indeed, the effects of inactivation of NF-κB signaling with the specific inhibitor, PDTC, resembled the cardioprotective effects of IκBα during H2O2 stimulation.Conclusion: IκBα overexpression can ameliorate H2O2-induced apoptosis, autophagy, oxidative injury, and ΔΨm loss through inhibition of the NF-κB signaling pathway. These findings suggest that IκBα transfection can successfully resist oxidative stress-induced damage through inhibiting NF-κB activation, which may provide a potential therapeutic target for prevention of myocardial I/R injury.

Protective Effect of SCUBE1 on Oxidative Stress-induced Apoptosis in Human Ovarian Granulosa Cells

2021 ◽  
Author(s):  
Huijiao Fu ◽  
Xuzi Cai ◽  
Qiwen Liu ◽  
Wei Yang ◽  
xuefeng wang
Keyword(s):  
Membrane Potential ◽  
Western Blot ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Granulosa Cells ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Cell Counting ◽  
Ovarian Granulosa Cells ◽  
Induced Apoptosis

Abstract Background: Apoptosis of ovarian granulosa cells (GCs) is a sign of follicular atresia. This study aimed to explore the role and mechanism of signal peptide, CUB domain, epidermal growth factor-like protein1 (SCUBE1) in protecting GCs from apoptosis induced by hydrogen peroxide (H2O2). Methods: Firstly, the expression of SCUBE1 on the ovaries of humans and mice was analyzed by qRT-PCR, western blot and immunohistochemistry. Subsequently, the H2O2 treated GCs were pretreated with SCUBE1 recombinant protein, and their cell viability and proliferation were detected by Cell Counting Kit-8 (CCK-8) assay. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) in the cells were determined by DCFH-DA and rhodamine 123, respectively. The percentage of apoptotic cells was analyzed by flow cytometry after staining with Annexin V/PI. The expression levels of pathway related proteins, such as Bcl-2, Bax, p53, caspase-3, were determined by western blot analysis. Finally, the pathogenicity of SCUBE1 (c.1169C>G, p.P390R) were analyzed based on the software.Results: SCUBE1 was expressed in women of all ages and had the highest expression level in the ovaries in multiple organs and tissues of KM mouse. In vitro cell experiments show that SCUBE1 pretreatment reduced H2O2-induced apoptosis and improved cell viability. SCUBE1 also blocked the production of ROS in cells and improved mitochondrial membrane potential. After SCUBE1 pretreatment, anti-apoptotic protein Bcl-2 expression was upregulated, whereas the expression of the pro-apoptotic proteins Bax, Bax/Bcl-2, Caspase-3, and p53 were downregulated. Analysis of the impact of SCUBE1 (c.1169C >G, p.P390R) mutation from the aspect of mutation pathogenicity; protein stability; and gene haplotype insufficiency, indicated that the p.P390R mutation is significantly pathogenic.Conclusions: This is the first time that the potential role of SCUBE1 in protecting GCs from H2O2-induced damage through the mitochondrial pathways, attributing to POI, is studied. SCUBE1 (c.1169C >G, p.P390R) mutation has significant pathogenicity but the specific harm needs to be confirmed by further studies. Trial registration: Not applicable.

scholarly journals circHUWE1 Exerts an Oncogenic Role in Inducing DDP-Resistant NSCLC Progression Depending on the Regulation of miR-34a-5p/TNFAIP8

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Xueliang Yang ◽  
Quan Sun ◽  
Yongming Song ◽  
Wenli Li
Keyword(s):  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Cell Cycle Distribution ◽  
Necrosis Factor Alpha ◽  
Induced Apoptosis

Background. Circular RNAs (circRNAs) are reported as competing endogenous RNAs (ceRNAs) and play key roles in non-small-cell lung cancer (NSCLC) progression. Thus, this study was aimed at clarifying underlying molecular mechanisms of circHUWE1 in NSCLC. Methods. The quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analyses were used for examining circHUWE1, microRNA-34a-5p (miR-34a-5p), and tumor necrosis factor alpha-induced protein 8 (TNFAIP8). IC50 of cisplatin (DDP) in A549/DDP and H1299/DDP cells and cell viability were analyzed by the Cell Counting Kit 8 (CCK-8) assay. Colony forming assay was performed to assess colony forming ability. Cell apoptosis and cell cycle distribution were determined by flow cytometry. Migrated and invaded cell numbers were examined by transwell assay. The association among circHUWE1, miR-34a-5p, and TNFAIP8 was analyzed by dual-luciferase reporter and RNA immunoprecipitation assays. A xenograft experiment was applied to clarify the functional role of circHUWE1 in vivo. Results. circHUWE1 was upregulated in NSCLC tissues and cells, especially in DDP-resistant groups. circHUWE1 downregulation inhibited DDP resistance, proliferation, migration, and invasion while it induced apoptosis and cell cycle arrest of DDP-resistant NSCLC cells, which was overturned by silencing of miR-34a-5p. TNFAIP8 was a functional gene of miR-34a-5p, and the suppressive effects of miR-34a-5p overexpression on DDP-resistant NSCLC progression were dependent on the suppression of TNFAIP8. circHUWE1 inhibition also delayed tumor growth of DDP-resistant NSCLC cells. Conclusion. circHUWE1 functioned as a promoter in DDP-resistant NSCLC by interaction with miR-34a-5p-TNFAIP8 networks, providing novel insight into DDP-resistant NSCLC diagnosis and treatment.

scholarly journals Resveratrol protects against apoptosis induced by interleukin-1β in nucleus pulposus cells via activating mTOR/caspase-3 and GSK-3β/caspase-3 pathways

2020 ◽  
Vol 40 (7) ◽  
Author(s):  
Xiaohui Guo ◽  
Xiaoliang Bai ◽  
Feng Zhang ◽  
Long Zheng ◽  
Wenyuan Ding ◽  
...  
Keyword(s):  
Western Blot ◽  
Nucleus Pulposus ◽  
Caspase 3 ◽  
Cell Activity ◽  
Cell Counting ◽  
Nucleus Pulposus Cells ◽  
Apoptosis Rate ◽  
Protein Levels ◽  
Gsk 3Β ◽  
Human Npcs

Abstract Objective: The purpose of the present study was to investigate the specific downstream signaling pathway mediated by PI3K/Akt in resveratrol (RES) anti-apoptosis of nucleus pulposus cells (NPCs). Materials and methods: Human NPCs were cultured and divided into six groups. Interleukin (IL)-1β was used to induce apoptosis and RES to inhibit apoptosis. Fluorescence-activated cell sorting (FACS) analysis was used to test apoptotic incidence of NPCs, cell counting kit-8 (CCK-8) assay was performed to detect cell viability, The expression level of caspase-3 mRNA was detected by RT-qPCR, and protein levels were determined by Western blot. Results: Flow cytometry analysis showed that IL-1β increased the apoptosis rate of NPCs in each group, and RES significantly decreased the apoptosis rate, while rapamycin (RAPA) and SB216763 inhibited the effect of RES and increased the apoptosis rate again. Similarly, CCK-8 showed that IL-1β decreased activity of NPCs in each group, while RES increased cell activity, RAPA and SB216763 inhibited the effect of RES and decreased cell activity. RT-qPCR results showed IL-1β significantly increased the level of caspase-3 expression, but it was significantly decreased by using RES, RAPA and SB216763 respectively attenuated effects of RES. Western blot results showed that activated caspase-3 was inhibited by RES effect, and was up-regulated again after the addition of RAPA and SB216763. In addition, p-mTOR and p-GSK-3β were up-regulated by RES and down-regulated by RAPA and SB216763. Conclusion: RES can inhibit apoptosis induced by IL-1β in human NPCs. PI3K/Akt/mTOR/caspase-3 and PI3K/Akt/GSK-3β/caspase-3 pathways are potential mechanisms underlying this process.

scholarly journals miRNA-103 promotes chondrocyte apoptosis by down-regulation of Sphingosine kinase-1 and ameliorates PI3K/AKT pathway in osteoarthritis

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Fang Li ◽  
Jianhua Yao ◽  
Qingqing Hao ◽  
Zheping Duan
Keyword(s):  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Sphingosine Kinase ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Chondrocyte Apoptosis ◽  
Sphingosine Kinase 1 ◽  
Down Regulation ◽  
Induced Apoptosis

Abstract Objectives: The aim of the present study was to determine the effects of miRNA-103 on chondrocyte apoptosis and molecular mechanisms in osteoarthritis (OA) progression. Methods: The cell proliferation, apoptosis, and recovery ability were measured by cell counting kit-8 (CCK-8), flow cytometry, and wound healing assays. The interaction of miRNA-103 and Sphingosine kinase-1 (SPHK1) were determined by using luciferase reporter assay. The expression of mRNA and proteins were measured by qRT-PCR and Western blot. OA rat model was established by surgery stimulation. Results: miRNA-103 expression was significantly increased in the cartilage of OA patients and surgery-induced OA rat models. miRNA-103 transfection into primary rat chondrocytes reduced SPHK1 expression, induced apoptosis, inhibited cell proliferation, and impeded scratch assay wound closure. Moreover, expression of total AKT, and p-AKT were significantly reduced in miRNA-103-overexpressing chondrocytes while SPHK1 up-regulation increased the expression of phosphatidylinsitol-3-kinase (PI3K) and p-AKT, and reversed the proliferation suppression induced by the miRNA-103 mimic. Conclusions: Our studies suggest that miRNA-103 contributes to chondrocyte apoptosis, promoting OA progression by down-regulation of PI3K/AKT pathway through the reduction in SPHK1 activity.

scholarly journals Circular RNA circ_0128846 promotes the progression of osteoarthritis by regulating miR-127-5p/NAMPT axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Chao Liu ◽  
Ping Cheng ◽  
Jianjun Liang ◽  
Xiaoming Zhao ◽  
Wei Du
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Circular Rna ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Western Blot Assay ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Ecm Degradation ◽  
Oa Chondrocytes

Abstract Background Mounting evidence indicates that circular RNAs (circRNAs) participate in the occurrence and development of various diseases, including osteoarthritis (OA). However, the effects and molecular mechanism of circ_0128846 in OA have not been reported. Methods The expression levels of circ_0128846, microRNA-127-5p (miR-127-5p), and nicotinamide phosphoribosyltransferase (NAMPT) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was examined by flow cytometry and western blot assay. Inflammatory response and cartilage extracellular matrix (ECM) degradation were evaluated by western blot assay. The relationship between miR-127-5p and circ_0128846 or NAMPT was predicted by bioinformatics tools and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. Results Circ_0128846 and NAMPT were upregulated and miR-127-5p was downregulated in OA cartilage tissues. Knockdown of circ_0128846 increased cell viability and inhibited apoptosis, inflammation and ECM degradation in OA chondrocytes, while these effects were reversed by downregulating miR-127-5p. Moreover, circ_0128846 positively regulated NAMPT expression by sponging miR-127-5p. Furthermore, miR-127-5p promoted cell viability and suppressed apoptosis, inflammation, and ECM degradation in OA chondrocytes by directly targeting NAMPT. Conclusion Circ_0128846 knockdown might inhibit the progression of OA by upregulating miR-127-5p and downregulating NAMPT, offering a new insight into the potential application of circ_0128846 in OA treatment.

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

2021 ◽  
Vol 8 ◽  
Author(s):  
Huan Wan ◽  
Ting You ◽  
Wei Luo
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Cell Viability ◽  
Vascular Endothelial Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Vascular Endothelial ◽  
The Status ◽  
Rna Immunoprecipitation

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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