Association of<i>lincRNA-p21</i>Haplotype with Coronary Artery Disease in a Chinese Han Population

Tang, Sai-sai; Cheng, Jie; Cai, Meiying; Yang, Xia; Liu, Xinguang; Zheng, Baodong; Xiong, Xing‐Dong

doi:10.1155/2016/9109743

Cited by 20 publications

(15 citation statements)

References 34 publications

(28 reference statements)

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“…However, little is known about their roles in the cardiovascular diseases. In a previous study, lincRNA-p21 played an important role in the pathogenesis and progression of coronary heart disease [17]. Moreover, lncRNA APF was crucial for the regulation of autophagic cell death and myocardial infarction by targeting miR-188-3p [18].…”

Section: Discussionmentioning

confidence: 91%

LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Rare studies have been conducted to investigate the exact interactions between lung adenocarcinoma transcript 1 (MALAT1), thymocyte selection-associated high mobility group box (TOX), and miRNAs in the pathogenesis of atherosclerosis (AS). We aim to investigate the crosstalk between MALAT1 and TOX and evaluate whether the regulatory mechanism was associated with the miRNA network. AS tissues were collected to determine the level of MALAT1 expression in AS patients, together with determination of miR-181b expression. Cultured endothelial cells were utilized to analyze the expressions of MALAT1, miR-181b, and TOX in the presence of oxLDL. Luciferase activity assay was conducted to evaluate the potential target sites of miR-181b on MALAT1 and TOX. In this study, we demonstrated that MALAT1 was upregulated in patients with AS. MALAT1 silencing significantly downregulated the expression of the miR-181b target gene TOX via reversing the effect of miR181b. Importantly, positive modulation of miR181b and inhibition of MALAT1 and TOX significantly attenuated oxLDL-induced endothelial inflammation and oxidative stress. Moreover, the MAPK signal pathways in endothelial cells were also inhibited through regulation of above endogenous RNAs. In summary, MALAT1 suppression protects the endothelium from oxLDL-induced inflammation and oxidative stress in endothelial cells by upregulation of miR-181b and downregulation of TOX.

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Section: Discussionmentioning

confidence: 91%

LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“… 78 Furthermore, polymorphisms in lincRNA-p21 have been associated with CAD risk. 79 The therapeutic potential of lncRNA-p21 in acute vascular injury is suggested by its regulatory role of cell proliferation and apoptosis in CAD.…”

Section: Main Textmentioning

confidence: 99%

The Function and Therapeutic Potential of Long Non-coding RNAs in Cardiovascular Development and Disease

Gomes

Spencer

Ford

et al. 2017

Molecular Therapy - Nucleic Acids

100

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The popularization of genome-wide analyses and RNA sequencing led to the discovery that a large part of the human genome, while effectively transcribed, does not encode proteins. Long non-coding RNAs have emerged as critical regulators of gene expression in both normal and disease states. Studies of long non-coding RNAs expressed in the heart, in combination with gene association studies, revealed that these molecules are regulated during cardiovascular development and disease. Some long non-coding RNAs have been functionally implicated in cardiac pathophysiology and constitute potential therapeutic targets. Here, we review the current knowledge of the function of long non-coding RNAs in the cardiovascular system, with an emphasis on cardiovascular development and biology, focusing on hypertension, coronary artery disease, myocardial infarction, ischemia, and heart failure. We discuss potential therapeutic implications and the challenges of long non-coding RNA research, with directions for future research and translational focus.

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“…In atherosclerosis, lincRNA-p21 has been identified to inhibit proliferation and induce apoptosis in vascular smooth muscle cells (15). in addition, the G-a-a-G haplotype of lincrna-p21 is correlated with a decreased risk of cad (16). CoroMarker (lncRNA AC100865.1), abhydrolase domain containing 16A, and IL21R antisense RNA 1 were identified by microarray and confirmed by reverse transcription-quantitative (RT-q) PCR in peripheral blood mononuclear cells (PBMCs) (17).…”

Section: Introductionmentioning

confidence: 99%

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

Yan

et al. 2020

Mol Med Report

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coronary artery disease (cad) is a serious threat to human health and a major cause of mortality worldwide. long noncoding rnas (lncrnas) affect the occurrence and development of cad via the regulation of cell proliferation and apoptosis, inflammatory responses and lipid metabolism. Screening methods and therapeutic strategies for cad have been extensively studied. The present study analyzed clinical indexes of 187 patients with CAD and 150 healthy subjects. The data showed significant differences in diabetes mellitus, hypertension, high-density lipoprotein level and smoking history between the CAD group and the control group. A series of differentially expressed lncRNAs were detected in the plasma samples of three patients with CAD by high-throughput sequencing. reverse transcription-quantitative (rT-q)Pcr data revealed that the expression level of the novel lncRNA enST00000416361 was ~2.3-fold higher in the plasma of 50 patients with CAD compared with the 50 control subjects. receiver operating characteristic (roc) curves were generated, and the area under the roc curve was 0.7902. Knockdown of ENST00000416361 in human umbilical vein endothelial cells markedly downregulated interleukin-6 and tumor necrosis factor-α levels. In addition, sterol regulatory element binding transcription factor (SreBP)1 and SreBP2 were upregulated in patients with cad, and they were positively correlated with the expression of ENST00000416361. RT-qPCR further demonstrated that knockdown of enST00000416361 led to the downregulation of SreBP1 and SreBP2. overall, the novel lncRNA ENST00000416361 may be associated with CAD-induced inflammation and lipid metabolism, and it may serve as a potential biomarker for CAD.

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Association oflincRNA-p21Haplotype with Coronary Artery Disease in a Chinese Han Population

Cited by 20 publications

References 34 publications

LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX

LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX

The Function and Therapeutic Potential of Long Non-coding RNAs in Cardiovascular Development and Disease

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

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