Knockdown of long noncoding RNA XIST alleviates oxidative low-density lipoprotein-mediated endothelial cells injury through modulation of miR-320/NOD2 axis

Xu, Xiaohui; Ma, Congmin; Liu, Chao; Duan, Zhihui; Zhang, Li

doi:10.1016/j.bbrc.2018.06.042

Cited by 39 publications

(21 citation statements)

References 31 publications

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“…As reported by Geng, ox-LDL stimulates the inflammation of monocytes by activating NF-κB and facilitating monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) production [18]. Moreover, ox-LDL contributes to HUVECs dysfunction and VSMCs calcification [10,19]. Consistent with previous studies, we also certified that ox-LDL treatment elicited HUVECs injury by suppressing cell viability.…”

Section: Discussionsupporting

confidence: 91%

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RETRACTED ARTICLE: SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis

et al. 2020

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Background: Plenty of long non-coding RNAs (lncRNAs) play vital roles in the progression of atherosclerosis. Small nucleolar RNA host gene 6 (SNHG6) is a well known lncRNA that is aberrantly high expressed in atherosclerosis patients. However, its function and basic mechanism in atherosclerosis events have not been well clarified. Methods: The expression patterns of SNHG6, miR-135a-5p, ROCK1 and ROCK2 in clinical samples and cells were detected by RT-qPCR assays. Cell Counting Kit-8 (CCK-8), flow cytometry assays, ELISA and reactive oxygen species (ROS) and malondialdehyde (MDA) detection, were performed to assess cell viability, apoptosis, inflammation and oxidative stress, respectively. Western blot analysis was carried out to examine the protein levels of Bax, Bcl-2, and SNHG6. Luciferase reporter and RIP assays were used to confirm the true interaction between SNHG6 and miR-135a-5p, or miR-135a-5p and ROCK. Results: The levels of SNHG6, ROCK1 and ROCK2 were notably increased and miR-135a-5p was decreased in atherosclerosis patients and oxidized low-density lipoprotein (ox-LDL)-treated HUVECs. Knockdown of SNHG6 alleviated ox-LDL-induced injury of HUVECs, while this effect was partly reversed by miR-135a-5p inhibitor. Moreover, overexpression of ROCKs aggravated miR-135a-5p-alleviated atherosclerosis cell injury. SNHG6 contributed to ROCK expression through sequestering miR-135a-5p as a molecular sponge. Conclusion: SNHG6 functions as a promoter in atherosclerosis events by targeting miR-135a-5p/ROCK axis in ox-LDLstimulated HUVECs. This finding will help to develop a novel therapeutic strategy for atherosclerosis.

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Section: Discussionsupporting

confidence: 91%

“…LincRNA-p21 exerts an atheroprotective role in atherosclerosis by recovering the function of VSMCs and mouse mononuclear macrophage cells [9]. Knockdown of lncRNA XIST partially alleviates ox-LDL-elicited ECs injury via regulation of miR-320/NOD2 axis [10].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis

et al. 2020

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“…lincRNA-p21 Stimulates ox-LDL-induced EC apoptosis and LOX-1 expression via activation of protein kinase C delta (PKCδ) that regulates atherosclerosis pathogenesis [232] TCONS_00024652 Promotes EC proliferation, migration and angiogenesis via downregulating miR21 expression that stimulates atherosclerosis progression [233] XIST Promotes ox-LDL-mediated EC injury via miR-320/ nucleotide binding oligomerization domain containing 2 (NOD2) pathway and modulates atherosclerosis [80] RNCR3…”

Section: Rp11-714g181mentioning

confidence: 99%

A Brief Overview of lncRNAs in Endothelial Dysfunction-Associated Diseases: From Discovery to Characterization

Islam

Lai

2019

Epigenomes

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Long non-coding RNAs (lncRNAs) are a novel class of regulatory RNA molecules and they are involved in many biological processes and disease developments. Several unique features of lncRNAs have been identified, such as tissue-and/or cell-specific expression pattern, which suggest that they could be potential candidates for therapeutic and diagnostic applications. More recently, the scope of lncRNA studies has been extended to endothelial biology research. Many of lncRNAs were found to be critically involved in the regulation of endothelial function and its associated disease progression. An improved understanding of endothelial biology can thus facilitate the discovery of novel biomarkers and therapeutic targets for endothelial dysfunction-associated diseases, such as abnormal angiogenesis, hypertension, diabetes, and atherosclerosis. Nevertheless, the underlying mechanism of lncRNA remains undefined in previous published studies. Therefore, in this review, we aimed to discuss the current methodologies for discovering and investigating the functions of lncRNAs and, in particular, to address the functions of selected lncRNAs in endothelial dysfunction-associated diseases.The disruptions of the auto-regulatory processes in endothelium, including decreased production and bioavailability of NO, impaired endothelial dependent-NO-mediated vascular relaxation, upregulated inflammatory genes expression level, dysregulated hemodynamic, adhesion molecules up-expression, excessive ROS production, and enhanced vascular endothelium permeability [3][4][5][6][7][8]. They are conclusively referred as "endothelial dysfunction (ED)". Subsequently, the dysfunction leads to the development and progression of different forms of vascular diseases [6]. Numerous studies have discovered significant correlations between ED and vascular-mediated diseases, such as angiogenesis, atherosclerosis, hypertension, diabetes, insulin resistance, obesity, etc. [6]. However, the underlying pathophysiology of ED and the correlations between functional roles of lncRNAs and vascular-mediated diseases remain unclear. Therefore, we aim to provide a brief playbook for the discovery and characterization of lncRNAs in ED-associated diseases and, in particular, to provide a concise overview of current knowledge on lncRNAs in ED-associated diseases. It is believed that with a better understanding the correlations of lncRNAs and ED-associated diseases, researches can make a positive impact on the development of novel biomarkers and therapeutic targets in ED-associated disease treatments. lncRNAs in the Regulation of Gene ExpressionAdvanced genome-and transcriptome-wide analyses discovered that <2% of human genome contains protein coding transcripts, while >75% of which were transcribed into noncoding RNAs (ncRNAs) and have no protein coding potentiality [9,10]. The ncRNAs can be broadly classified into two groups based upon their sizes: the short noncoding RNAs which are less than 200 nucleotides (nt) in length, such as small interfering RNAs (siRNAs), small nu...

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“…The role of lncRNA in angiogenesis and EC dysfunction has also been investigated [12,13]. LncRNA XIST was shown to induce oxLDL-treated EC injury by regulating the miR-320/NOD2 pathway [14]. LncRNA H19 contributes to oxLDL-treated EC injury via miR-let-7/periostin.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA NEAT1 inhibits oxidative stress-induced vascular endothelial cell injury by activating the miR-181d-5p/CDKN3 axis

Zhang

Wang

Yao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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show abstract

Knockdown of long noncoding RNA XIST alleviates oxidative low-density lipoprotein-mediated endothelial cells injury through modulation of miR-320/NOD2 axis

Cited by 39 publications

References 31 publications

RETRACTED ARTICLE: SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis

RETRACTED ARTICLE: SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis

A Brief Overview of lncRNAs in Endothelial Dysfunction-Associated Diseases: From Discovery to Characterization

Long non-coding RNA NEAT1 inhibits oxidative stress-induced vascular endothelial cell injury by activating the miR-181d-5p/CDKN3 axis

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