Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX–1 signalling pathway

Xu, Kang; liu, Xiwen; Ren, Guanghao; Yin, Di; Guo, Suli; Zhao, Yue

doi:10.1016/j.lfs.2019.116874

Cited by 14 publications

(10 citation statements)

References 34 publications

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“…Atherosclerosis is a growing threat to human health, and the dysfunction of VSMcs has been reported to be involved in the formation of atherosclerosis (28,29). In the present study, VSMcs were treated with ox-LdL to establish the cell model for atherosclerosis based on previous studies (29,30). Recently, circRNAs have been identified to serve a pivotal role in various human diseases.…”

Section: Discussionmentioning

confidence: 99%

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

Tian

et al. 2020

Int J Mol Med

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Atherosclerosis is a disease during which the inside of an artery narrows due to the accumulation of plaque, and vascular smooth muscle cells (VSMcs) are involved in the progression of atherosclerosis. circular RNAs (circRNAs) have been reported to be involved in the progression of atherosclerosis. However, the role of circ_0010283 in atherosclerosis progression remains unclear. The present study aimed to investigate the functions and the mechanism of circ_0010283 in oxidized low-density lipoprotein (ox-LdL)-induced VSMcs and to identify new potential biomarkers for the treatment of atherosclerosis. cell viability and migration were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. The relationship between microRNA (miR)-370-3p and circ_0010283 or high mobility group box 1 (HMGB1) was predicated by online software and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. The results of the present study demonstrated that the expression levels of circ_0010283 and HMGB1 were significantly upregulated in ox-LdL-induced VSMcs compared with those in VSMcs without ox-LdL induction, whereas the expression of miR-370-3p was downregulated. Knockdown of circ_0010283 suppressed VSMc viability and migration, as well as the expression of viability-associated proteins cyclin d1 and proliferating cell nuclear antigen, and migration-associated proteins matrix metalloproteinase 2 (MMP2) and MMP9 in ox-LdL-induced VSMcs compared with untreated VSMcs. In addition, miR-370-3p was demonstrated to be a target of circ_0010283 and to target HMGB1; thus, circ_0010283 regulated HMGB1 expression via miR-370-3p. Further experiments indicated that inhibition of miR-370-3p reversed the circ_0010283 silencing-mediated inhibitory effects on VMSc viability and migration. Additionally, the miR-370-3p-mediated suppressive effects on cell viability and migration were rescued by overexpression of HMGB1. In conclusion, circ_0010283 mediated cell viability and migration via a miR-370-3p/HMGB1 axis in ox-LdL-induced VSMcs.

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Section: Discussionmentioning

confidence: 99%

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

Tian

et al. 2020

Int J Mol Med

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“…Furthermore, endothelial-mesenchymal transition (EndMT) helps endothelial cells to acquire a mesenchymal phenotype ( 9 ). Oxidized low-density lipoprotein (Ox-LDL) is a common factor in the establishment of experimental models of atherosclerosis, which may induce endothelial cell apoptosis and act as an essential risk factor for the formation of atherosclerosis ( 10 , 11 ).…”

Section: Introductionmentioning

confidence: 99%

SESN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling

et al. 2022

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endothelial cells are an important component of the heart and vasculature and form a crucial link between the cardiovascular system and the immune system. Sestrin 1 (SeSn1) has an important role in atherosclerosis by inhibiting NOD-like receptor family pyrin domain containing 3 inflammasome activation. However, whether SeSn1 is involved in human umbilical vein endothelial cell (HuVec) injury caused by atherosclerosis has remained to be elucidated. The present study aimed to investigate the functions of SeSn1 in the inflammatory response, apoptosis and endothelial-mesenchymal transition (endMT) of HuVecs following stimulation with oxidized low-density lipoprotein (ox-ldl). SeSn1 expression at the mrna and protein levels was detected using reverse transcription-quantitative Pcr (rT-qPcr) and western blot analysis. Following SeSn1 overexpression in ox-ldl-stimulated HuVecs, cell viability was determined using a cell counting Kit-8 assay. Terminal deoxynucleotidyl transferase-mediated nick-end labeling staining was employed to detect cell apoptosis and western blot analysis was used to determine the levels of apoptosis-related proteins. rT-qPcr, eliSa and western blot were utilized to determine the levels of inflammatory factors. immunofluorescence staining, rT-qPcr and western blot analysis were employed to assess the endMT of ox-ldl-stimulated HuVecs. The results revealed that SeSn1 exhibited a low expression in HuVecs following ox-ldl stimulation. SeSn1 overexpression suppressed inflammation, apoptosis and EndMT in ox-ldl-induced HuVecs. in addition, SeSn1 stimulated adenosine monophosphate-activated protein kinase catalytic subunit α1/sirtuin 1 signaling to suppress ox-ldl receptor-1 expression. an aMPK and SirT1 inhibitor reversed the effects of SESN1 overexpression on the inflammatory response, apoptosis and endMT of HuVecs exposed to ox-ldl. Taken together, the present study demonstrated that SenS1 exerts a suppressive effect on Ox-LDL-induced inflammation, apoptosis and endMT of HuVecs, suggesting that SenS1 may be used as a novel biomarker for endothelial injury-related disorders.

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“…37 In the injured endothelial cells, the expression of SIRT1 is inhibited, which suggests that SIRT1 may be involved in vascular endothelial injury. 38 In gouty arthritis and hyperinsulinemia, SIRT1 suppresses the inflammatory infiltration, indicating that SIRT1 is a protective factor in inflammatory situations. 39,40 All aforementioned results confirmed that SIRT1 manipulated the function of HUVEC and its effect under the control of miR-128-3p.…”

Section: Discussionmentioning

confidence: 99%

MiR-128-3p promotes the progression of deep venous thrombosis through binding SIRT1

Han

et al. 2023

Phlebology

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Objectives This research aimed to study the effect of microRNA-128-3p (miR-128-3p) on deep venous thrombosis (DVT). Method The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Transwell chamber method, and flow cytometry technique were used in the cell experiments. Potential interconnection between miR-128-3p and silent information regulator sirtuin 1 (SIRT1) was revealed by luciferase activity. The concentration of miR-128-3p and mRNA SIRT1 was assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The receiver operating characteristic (ROC) curve was used to test the predictive effect of miR-128-3p in DVT. Results Decreased miR-128-3p expression was beneficial to cell proliferation and migration and inhibited inflammation, apoptosis, and adhesion of human umbilical vein endothelial cells (HUVECs). The impacts of miR-128-3p on HUVECs were achieved by targeting SIRT1. MiR-128-3p was upregulated in patients with DVT, and it was of great significance in differentiating patients with DVT. Conclusion Overexpression of miR-128-3p might become a biomarker for patients with DVT.

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Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX–1 signalling pathway

Cited by 14 publications

References 34 publications

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

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

SESN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling

MiR-128-3p promotes the progression of deep venous thrombosis through binding SIRT1

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