miR‑454‑3p prevents ox‑LDL‑induced apoptosis in HAECs by targeting TRPC3

Liao, Luming; Yang, Qing; Li, Hailiang; Wang, Mengqi; Li, Yuntian

doi:10.3892/etm.2021.9754

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…17 Furthermore, TRPC3 could promote atherosclerosis progression through increasing ox-LDL-induced aortic endothelial cell damage. 18 Our study predicted TRPC3 might act as a target of miR-137 by TargetScan online tool. Nevertheless, little is known about if miR-137 could regulate TRPC3 to control VSMC proliferation and migration.…”

mentioning

confidence: 76%

“…Transient receptor potential cation channel subfamily C member 3 (TRPC3) is widely expressed in many cell types including smooth muscle cells of vascular tissues, 16 and it appears to regulate functions of cardiovascular system 17 . Furthermore, TRPC3 could promote atherosclerosis progression through increasing ox‐LDL‐induced aortic endothelial cell damage 18 . Our study predicted TRPC3 might act as a target of miR‐137 by TargetScan online tool.…”

Section: Introductionmentioning

confidence: 85%

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Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox‐LDL through the miR‐137/TRPC3 axis

Gao

Guan

2023

The Kaohsiung J of Med Scie

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Tanshinone IIA (Tan IIA) has an important role in treatment of cardiovascular diseases, including atherosclerosis. The vascular smooth muscle cells (VSMCs) are a major part of the atherosclerotic plaque. However, the biological functions of Tan IIA in regulating VSMCs function remain mostly unclear. This research aimed at identifying the explicit molecular mechanism that Tan IIA regulates oxidized low‐density lipoprotein (ox‐LDL)‐mediated VSMC proliferation and migration. VSMCs challenged by ox‐LDL were adopted as cellular model of atherosclerosis, and suffered from Tan IIA treatment. After that, cells proliferation, apoptosis or migration were measured. The expression levels of microRNA (miR)‐137, transient receptor potential cation channel subfamily C member 3 (TRPC3) and proliferating cell nuclear antigen (PCNA) were measured. The targeting relationship between miR‐137 and TRPC3 was determined. It was found that Tan IIA blunted VSMC proliferation, PCNA expression and migration mediated by ox‐LDL. Tan IIA promoted miR‐137 level, and miR‐137 knockdown reversed the influences of Tan IIA on VSMC proliferation, PCNA expression and migration in the presence of ox‐LDL. TRPC3 was verified to be targeted by miR‐137. Moreover, TRPC3 silencing exacerbated the influences of Tan IIA on VSMC proliferation, apoptosis and migration, and it mitigated the inhibitive effects of miR‐137 knockdown on function of Tan IIA. We confirmed for the first time that Tan IIA constrained ox‐LDL‐stimulated VSMC proliferation and migration via regulating the miR‐137/TRPC3 axis, which provided a theoretical basis for the research and promotion of Tan IIA as a therapeutic drug.

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mentioning

confidence: 76%

Section: Introductionmentioning

confidence: 85%

Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox‐LDL through the miR‐137/TRPC3 axis

Gao

Guan

2023

The Kaohsiung J of Med Scie

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“…40 Meanwhile, the miR-454-3p suppression attenuated the viability of human aortic endothelial cells, while overexpression of miR-454-3p inhibited the apoptosis of HAEC-induced ox-LDL, thereby affecting the apoptosis of endothelial cells. 41 Transmembrane gammacarboxyglutamic acid protein 4 (PRRG 4), a protein-coding gene has been proved to promote the progression of breast cancer, and enhance metastasis. 42 It can also promote autism symptoms of WAGR by perturbing these mechanisms in the developing human brain.…”

mentioning

confidence: 99%

Comprehensive Analysis of a Competing Endogenous RNA Co-Expression Network in Chronic Obstructive Pulmonary Disease

Wang,

Xia,

et al. 2023

COPD

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Chronic obstructive pulmonary disease (COPD) is the main cause of mortality world widely. Non-coding RNAs (lncRNAs) and associated competitive endogenous RNAs (ceRNAs) networks were recently proved to lead to mRNA gene expression downregulation but were still unclear in COPD. This study aims to investigate and elucidate the mechanisms underlying the involvement of ceRNA co-expression networks in COPD pathogenesis. Methods: Obtained expression signature of data from the Gene Expression Omnibus database and compared the differentially expression of mRNAs and miRNAs between COPD patients and healthy smokers. Predicted the miRNA-lncRNA and miRNA-mRNA interaction using online library and employed CIBERSORT to measure the proportions of the 22 immune cells in the COPD and control groups. Results: Established a ceRNA-network comprising 11 lncRNAs, 5 miRNAs, and 16 mRNAs. Using the weighted correlation network analysis method, we identified hub genes and hub miRNAs and obtained one core sub-network, XIST, FGD5-AS1, KCNQ1OT1, HOXA11-AS, LINC00667, H19, PRKCQ-AS1, NUTM2A-AS1/has-mir-454-3p/ZNF678, PRRG4. COPD patients had different proportions of immune cells than controls, and these variations were associated with the magnitude of pulmonary function parameters. Conclusion:The ceRNA-network, particularly the core sub-network, may be a putative goal for COPD, in which specific immune cells were involved.

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Circ_0093887 regulated ox-LDL induced human aortic endothelial cells viability, apoptosis, and inflammation through modulating miR-758-3p/BAMBI axis in atherosclerosis

Wang¹,

Chen

et al. 2022

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BACKGROUND: Compelling evidence demonstrated that circular RNAs (circRNAs) were involved in the progression of atherosclerosis (AS). However, the role of circ_0093887 in the progression of AS is unclear. The purpose of this study was to explore the role and mechanism of circ_0093887 in oxidized-low density lipoprotein (ox-LDL)-induced human aortic endothelial cells (HAECs). METHODS: HAECs were stimulated by ox-LDL to simulate AS-like injury in vitro. Circ_0093887, microRNA-758-3p (miR-758-3p), and BMP And Activin Membrane-Bound Inhibitor (BAMBI) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). PCNA, Bax, Bcl-2, and BAMBI protein levels were detected by western blot. Cell viability and apoptosis were examined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Tube formation assay was used to assess tube formation. The levels of inflammatory factors TNF-α and IL-1β were detected by corresponding ELISA kits. The relationship between miR-758-3p and circ_0093887 or BAMBI was tested via dual-luciferase reporter analysis and RNA immunoprecipitation. Oxidative stress related indexes (ROS and MDA) were detected by corresponding kits. RESULTS: The expression levels of circ_0093887 and BAMBI were prominently downregulated in ox-LDL-induced HAECs compared with control, whereas the expression of miR-758-3p was upregulated. Overexpression of circ_0093887 promoted HAECs viability and tube formation, and restrained cell apoptosis in ox-LDL-induced HAECs compared with untreated HAECs. Mechanistically, circ_0093887 regulated the expression of BAMBI through miR-758-3p. Further experiments showed that upregulation of miR-758-3p reversed changes in cell function induced by circ_0093887. In addition, reduced BAMBI salvaged miR-758-3p knockdown mediated effects on cell function. CONCLUSION: Circ_0093887 demonstrated its diagnostic and therapeutic value in AS by promoting the role of the miR-758-3p/BAMBI axis in the ox-LDL-induced endothelial injury of HAECs.

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miR‑454‑3p prevents ox‑LDL‑induced apoptosis in HAECs by targeting TRPC3

Cited by 5 publications

References 33 publications

Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox‐LDL through the miR‐137/TRPC3 axis

Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox‐LDL through the miR‐137/TRPC3 axis

Comprehensive Analysis of a Competing Endogenous RNA Co-Expression Network in Chronic Obstructive Pulmonary Disease

Circ_0093887 regulated ox-LDL induced human aortic endothelial cells viability, apoptosis, and inflammation through modulating miR-758-3p/BAMBI axis in atherosclerosis

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