[Retraction]MicroRNA-134 Promotes the Development of Atherosclerosis Via the ANGPTL4/LPL Pathway in Apolipoprotein E Knockout Mice

Ye, Qiong; Tian, Guo-Ping; Cheng, Hai-Peng; Zhang, Xin; Ou, Xiang; Yu, Xiao-Hua; Tan, Ru-Qi; Yang, Feng-Yun; Gong, Duo; Huang, Chong; Pan, Yan-Jun; Zhang, Jie; Chen, Ling-Yan; Zhao, Zhen-Wang; Xie, Wei; Li, Liang; Zhang, Min; Xia, Xiao-Dan; Zheng, Xi-Long; Tang, Chao-Ke

doi:10.5551/jat.40212

Cited by 22 publications

(17 citation statements)

References 31 publications

(40 reference statements)

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“…PCSK9 deficiency in dyslipidemic mice decreases expression of endothelial chemotactic factors that promote monocyte adhesion and infiltration into the vessel (7). On the other hand, suppression of ANGPTL3 may induce local pro-inflammatory effects in the vascular wall by increasing endothelial lipase and lipoprotein lipase local activity (11,12). In the present study, double and triple administration of the drugs decreased endothelial expression of ICAM-1, thus reducing monocyte adhesion to the vascular endothelium and appearing to improve markers of plaque stability to a similar extent.…”

supporting

confidence: 45%

ANGPTL3, PCSK9, and statin therapy drive remarkable reductions in hyperlipidemia and atherosclerosis in a mouse model

Hurt-Camejo

2020

Journal of Lipid Research

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supporting

confidence: 45%

ANGPTL3, PCSK9, and statin therapy drive remarkable reductions in hyperlipidemia and atherosclerosis in a mouse model

Hurt-Camejo

2020

Journal of Lipid Research

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“…For instance, miR‐19a can promote vascular inflammation and foam cell formation through targeting HBP‐1 in AS . miR‐134 promotes AS development via the ANGPTL4/LPL pathway in apolipoprotein E knockout mice . miR‐9 represses NLRP3 inflammasome activation in AS inflammation cell models through the JAK1/STAT pathway .…”

Section: Discussionmentioning

confidence: 99%

NEAT1 contributes to ox‐LDL‐induced inflammation and oxidative stress in macrophages through inhibiting miR‐128

et al. 2018

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Long noncoding RNAs (lncRNA) have been recognized as significant regulators in the progression of atherosclerosis (AS). Oxidized low-density lipoprotein (ox-LDL) can induce macrophage inflammation and oxidative stress, that serves important roles in AS. However, the exact function of lncRNA NEAT1 and its possible molecular mechanism in AS remain unclear. Here, we concentrated on the roles and molecular mechanisms of NEAT1 in AS development. In our current study, we observed that NEAT1 was elevated by ox-LDL in a dose-dependent and time-dependent manner. RAW264.7 cell survival was greatly enhanced, and cell apoptosis was significantly inhibited by LV-shNEAT1 transfection. In addition, knockdown of NEAT1 in RAW264.7 cells repressed CD36 expression and foam cell formation while NEAT1 overexpression shown an opposite process. Moreover, NEAT1 downregulation inhibited inflammation molecules including IL-6, IL-1β, and TNF-α. Meanwhile, silencing of NEAT1 can also suppress reactive oxygen species (ROS) and malondialdehyde (MDA) levels with an enhancement of superoxide dismutase (SOD) activity in RAW264.7 cells. MicroRNAs are some short RNAs, and they can regulate multiple biological functions in many diseases including AS. Here, we found that miR-128 expression was remarkably decreased in ox-LDL-incubated RAW264.7 cells. Interestingly, miR-128 mimics was able to reverse AS-correlated events induced by overexpression of NEAT1. By using bioinformatics analysis, miR-128 was predicted as a target of NEAT1 and the correlation between them was validated in our study. Taken these together, it was implied that NEAT1 participated in ox-LDL-induced inflammation and oxidative stress in AS development through sponging miR-128.

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“…Moreover, miR-134 has been shown to directly bind the 3' UTR of ANGPTL4 and supress its expression within macrophages which inadvertently permits enhanced lipoprotein lipase activity and subsequent foam cell formation alongside heightened pro-inflammatory cytokine release 162 . Accordingly, systemic administration of a miR-134 agomir increased aortic atherosclerotic plaque size in Apoedeficient mice which was associated with decreased ANGPTL4 levels and concomitant increased expression and activity of lipoprotein lipase and lipid content within plaques, whilst opposing effects were observed in mice which received a miR-134 antagomir 163 . miR-146: Elevated levels of miR-146 have been detected within human aortic and femoral artery atherosclerotic plaques 97 , and a single nucleotide polymorphism in the miR146a gene which alters miR-146a expression has been proposed as an indicator of coronary artery disease susceptibility 164 .…”

Section: Macrophages Mir-10mentioning

confidence: 98%

Non-coding RNAs in cardiovascular cell biology and atherosclerosis

Fasolo

Gregoli

Maegdefessel

et al. 2019

Cardiovascular Research

106

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Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the interaction of distinct and over-lapping mechanisms which dictate the roles and actions of multiple resident and recruited cell types including endothelial cells, vascular smooth muscle cells, and monocyte/macrophages. The discovery of non-coding RNAs (ncRNAs) including microRNAs, long non-coding RNAs, and circular RNAs, and their identification as key mechanistic regulators of mRNA and protein expression has piqued interest in their potential contribution to atherosclerosis. Accruing evidence has revealed ncRNAs regulate pivotal cellular and molecular processes during all stages of atherosclerosis including cell invasion, growth, and survival; cellular uptake and efflux of lipids, expression and release of pro- and anti-inflammatory intermediaries, and proteolytic balance. The expression profile of ncRNAs within atherosclerotic lesions and the circulation have been determined with the aim of identifying individual or clusters of ncRNAs which may be viable therapeutic targets alongside deployment as biomarkers of atherosclerotic plaque progression. Consequently, numerous in vivo studies have been convened to determine the effects of moderating the function or expression of select ncRNAs in well-characterized animal models of atherosclerosis. Together, clinicopathological findings and studies in animal models have elucidated the multifaceted and frequently divergent effects ncRNAs impose both directly and indirectly on the formation and progression of atherosclerosis. From these findings’ potential novel therapeutic targets and strategies have been discovered which may pave the way for further translational studies and possibly taken forward for clinical application.

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[Retraction]MicroRNA-134 Promotes the Development of Atherosclerosis Via the ANGPTL4/LPL Pathway in Apolipoprotein E Knockout Mice

Cited by 22 publications

References 31 publications

ANGPTL3, PCSK9, and statin therapy drive remarkable reductions in hyperlipidemia and atherosclerosis in a mouse model

ANGPTL3, PCSK9, and statin therapy drive remarkable reductions in hyperlipidemia and atherosclerosis in a mouse model

NEAT1 contributes to ox‐LDL‐induced inflammation and oxidative stress in macrophages through inhibiting miR‐128

Non-coding RNAs in cardiovascular cell biology and atherosclerosis

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