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

Wan, Huan; You, Tingting; Luo, Wei

doi:10.3389/fcvm.2021.646832

Cited by 24 publications

(12 citation statements)

References 40 publications

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“…Moreover, previous studies reported that circ_0003214 attenuated the capacities of proliferation, migration and angiogenesis in ox-LDL-administered human aorta endothelial cells (HAECs) and HUVECs [22,23]. In addition, circ_0003204 silencing was also demonstrated to suppress oxidative stress and inflammatory responses in ox-LDL-treated HUVECs [24]. Consistent with these findings, our data manifested that circ_0003204 deficiency alleviated ox-LDL-induced inflammation, cell viability inhibition, cell apoptosis and tube formation inhibition of HUVECs.…”

Section: Discussionsupporting

confidence: 90%

Circ_0003204 knockdown protects endothelial cells against oxidized low-density lipoprotein-induced injuries by targeting the miR-491-5p-ICAM1 pathway

Zhang

et al. 2021

J Thromb Thrombolysis

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Emerging evidence indicates that circular RNA (circRNA) is implicated in the development of atherosclerosis (AS). This study investigated the effect of circ_0003204 on endothelial cell function and explored the functional mechanism of circ_0003204 in AS progression. AS cell models were constructed by treating human umbilical vein endothelial cells (HUVEC) with oxidized low-density lipoprotein (ox-LDL). The expression of circ_0003204 was detected by quantitative real-time PCR (qPCR). The releases of pro-inflammatory factors were determined by ELISA. Cell viability was checked by CCK-8 assay. Cell apoptosis was monitored by flow cytometry assay. The ability of angiogenesis was assessed by tube formation assay. The protein levels of cell development-and apoptosis-related markers were measured by western blot. The binding relationship between miR-491-5p and circ_0003204 or intercellular adhesion molecule 1 (ICAM1) was verified by dual-luciferase reporter assay or RIP assay. The expression of circ_0003204 was strengthened in ox-LDL-treated HUVECs. Circ_0003204 knockdown inhibited ox-LDL-induced inflammation and cell apoptosis, and promoted ox-LDL-depleted cell viability and tube formation ability in HUVECs. MiR-491-5p was a target of circ_0003204, and miR-491-5p directly bound to ICAM1 3′UTR. Accordingly, circ_0003204 positively regulated ICAM1 expression by targeting miR-491-5p. Rescue experiments presented that miR-491-5p inhibition reversed the effects of circ_0003204 knockdown, and ICAM1 overexpression abolished the effects of miR-491-5p restoration. Circ_0003204 knockdown protects HUVECs against ox-LDL-induced injuries by targeting the miR-491-5p-ICAM1 pathway, hinting that circ_0003204 inhibition might prevent AS development. Keywords Circ_0003204 • miR-491-5p • ICAM1 • ox-LDL • HUVEC • Atherosclerosis Highlights• Circ_0003204 is upregulated in ox-LDL-treated HUVECs. • Circ_0003204 knockdown inhibits ox-LDL-induced HUVEC injuries. • Circ_0003204 regulates the miR-491-5p-ICAM1 pathway.

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Section: Discussionsupporting

confidence: 90%

Circ_0003204 knockdown protects endothelial cells against oxidized low-density lipoprotein-induced injuries by targeting the miR-491-5p-ICAM1 pathway

Zhang

et al. 2021

J Thromb Thrombolysis

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“…According to previous studies, miR-942-5p could attenuate oxidative stress and inflammation in an in vivo atherosclerosis model. 38 IgG Fcγ receptors are encoded by FCGR3A and FCGR3B, which in turn mediate immune cell activation promoting inflammation. 39 Regrettably, there is no evidence in the literature that the RNA molecules described above may be involved in the neuroinflammation of AIS.…”

Section: Discussionmentioning

confidence: 99%

Construction of circRNA-Mediated Immune-Related ceRNA Network and Identification of Circulating circRNAs as Diagnostic Biomarkers in Acute Ischemic Stroke

Wang¹,

Li²,

Liu³

et al. 2022

JIR

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Accumulating evidence suggests that circular RNAs (circRNAs) are involved in immune and inflammatory processes after acute ischemic stroke (AIS). However, the roles of circRNA-mediated competing endogenous RNA (ceRNA) in modulating immune inflammation of AIS have not yet been determined. This study aimed to construct a circRNA-mediated immunerelated ceRNA network and identify novel circRNAs in AIS. Methods: Microarray data were downloaded from the GEO database and further analysed by R software. Then, we constructed a circRNA-mediated ceRNA network based on interaction information from the bioinformatics database. A topological property analysis of the ceRNA network was conducted to screen novel circRNAs. Finally, we further applied quantitative real-time polymerase chain reaction (qRT-PCR) to two independent sets. Results: We constructed an AIS immune-related ceRNA (AISIRC) network containing immune-related genes (IRGs), miRNAs, and circRNAs. Additionally, we extracted the subnetwork from the AISIRC network and screened six immune-related circRNAs. After identification and validation, we finally confirmed that plasma levels of circPTP4A2 and circTLK2 were significantly increased in AIS patients compared with both healthy control subjects (HCs) and transient ischemic attack (TIA) patients. Logistic regression and receiver-operating characteristic (ROC) curve analyses demonstrated that these two circRNAs may function as predictive and discriminative biomarkers for AIS. We also confirmed that plasma levels of circPTP4A2 were elevated in TIA patients compared with HCs and might be an independent risk factor for predicting TIA. Longitudinal analysis of circRNA expression up to 90 days after AIS indicated that the ability of circPTP4A2 and circTLK2 to monitor AIS dynamics was highly desirable. Conclusion: In summary, the circRNA-mediated immune-related ceRNA network was successfully constructed, and two circulating circRNAs (circPTP4A2 and circTLK2) improved sensitivity for the diagnosis of AIS and could be considered diagnostic biomarkers.

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“…It is suggested that TTTY15 may be involved in the pathogenesis of diabetic nephropathy by targeting and regulating the expression of miR-942-5p. miR-942-5p has been shown to be poorly expressed in oxidative-Low Density Lipoprotein (ox-LDL) induced endothelial cell injury and up-regulation of miR-942-5p expression reduces ox-LDL-induced endothelial cell injury [16] . miR-942-5p is poorly expressed in adriamycin-induced cardiomyocytes and up-regulation of miR-942-5p expression inhibits doxorubicin-induced cardiomyocyte apoptosis [17] .…”

Section: Resultsmentioning

confidence: 99%

Study on Mechanism of Long Non-Coding RNA TTTY15 Targeting MicroRNA-942-5p Mediating High Glucose-Induced Renal Tubular Epithelial Cell Injury

Ma¹,

Qian²,

Luo³

et al. 2022

IJPS

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To investigate the effect of long non-coding RNA TTTY15 on high glucose-induced renal tubular epithelial cell injury and its possible mechanism. Human renal tubular epithelial cells HK-2 were induced by high glucose to establish cell injury model. Small molecule interfering-negative control, small molecule interfering-RNA gene TTTY15, microRNA-negative control, miR-942-5p mimics, small molecule interfering-RNA gene TTTY15 and anti-microRNA-negative control, small molecule interfering-RNA gene TTTY15 and anti-miR-942-5p were transfected into HK-2 cells by liposome transfection method and then treated with 25 mmol/l glucose for 24 h. The expression of TTTY15 and microRNA-942-5p was detected by quantitative real time polymerase chain reaction; the levels of interleukin-6 and tumor necrosis factor-alpha in the supernatant were detected by enzyme-linked immunosorbent assay; apoptosis rate was detected by flow cytometry. Dual-luciferase report assay verified the targeted regulation relationship between TTTY15 and microRNA-942-5p; the expression of cleaved caspase-3 and cleaved caspase-9 proteins was detected by Western blot. The expression of TTTY15 increased (p<0.05) and microRNA-942-5p decreased (p<0.05) in HK-2 cells induced by high glucose; transfection of small molecule interfering-RNA gene TTTY15 or microRNA-942-5p mimics could decrease the levels of interleukin-6, tumor necrosis factor-alpha (p<0.05), apoptosis, cleaved caspase-3 and cleaved caspase-9 proteins in HK-2 cells induced by high glucose (p<0.05); TTTY15 can regulate the expression of microRNA-942-5p; co-transfection of small molecule interfering-RNA gene TTTY15 and anti-miR-942-5p decreased the effect of small molecule interfering-RNA gene TTTY15 on inflammatory reaction and apoptosis induced by high glucose in HK-2 cells. Interference with TTTY15 expression may attenuate high glucose-induced tubular epithelial cell injury by targeting microRNA-942-5p expression and inhibiting the inflammatory reaction and apoptosis.

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

Cited by 24 publications

References 40 publications

Circ_0003204 knockdown protects endothelial cells against oxidized low-density lipoprotein-induced injuries by targeting the miR-491-5p-ICAM1 pathway

Circ_0003204 knockdown protects endothelial cells against oxidized low-density lipoprotein-induced injuries by targeting the miR-491-5p-ICAM1 pathway

Construction of circRNA-Mediated Immune-Related ceRNA Network and Identification of Circulating circRNAs as Diagnostic Biomarkers in Acute Ischemic Stroke

Study on Mechanism of Long Non-Coding RNA TTTY15 Targeting MicroRNA-942-5p Mediating High Glucose-Induced Renal Tubular Epithelial Cell Injury

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