Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis

Peng, Yudong; Meng, Kai; Jiang, Lili; Zhong, Yucheng; Yong, Yang; Lan, Yin; Zeng, Qiutang; Cheng, Long

doi:10.1042/bsr20170351

Cited by 60 publications

(36 citation statements)

References 28 publications

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“…Our initial quantitative real‐time RT‐PCR (qPCR) analysis included atherosclerosis‐ or cardiac‐related lncRNAs: lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), hypoxia‐inducible factor 1 alpha‐antisense RNA2 (HIF1A‐AS2) and apolipoprotein A‐1 antisense RNA (APOA1‐AS) . As illustrated, the three lncRNAs were significantly higher in PBMC samples from CAD patients than in those from healthy subjects.…”

Section: Resultsmentioning

confidence: 99%

KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS are promising novel biomarkers for diagnosis of coronary artery disease

Zhang

Wang

et al. 2019

Clin Exp Pharma Physio

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This study aimed to evaluate the potential of long noncoding RNAs (lncRNAs) as biomarkers for coronary artery disease (CAD). We measured the levels of three atherosclerosis‐ or cardiac‐related lncRNAs in peripheral blood monocyte cells (PBMCs) from 20 CAD patients and 20 non‐CAD control participants using real‐time reverse transcription–polymerase chain reaction (real‐time RT–PCR) methods. We found that the levels of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), hypoxia‐inducible factor 1 alpha‐antisense RNA 2 (HIF1A‐AS2) and apolipoprotein A‐1 antisense RNA (APOA1‐AS) were significantly increased in CAD patients (KCNQ1OT1 increased by 2.38‐fold, P = 0.00042; HIF1A‐AS2 increased by 2.00‐fold, P = 0.0001; APOA1‐AS increased by 4.52‐fold, P = 0.000048). The area under the ROC curve was 0.865 for KCNQ1OT1, 0.852 for HIF1A‐AS2, and 0.967 for APOA1‐AS. Furthermore, the combination of lncRNAs resulted in a much higher AUC value of 0.990 for the prediction of CAD. Spearman's correlation analysis showed that APOA1‐AS was positively correlated with NT‐proBNP, CKMB, MYO and HsTnT, whereas HIF1A‐AS2 was correlated with NT‐proBNP and HsTnT. Hence, the elevation of KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS predicts CAD and these molecules may be considered as novel biomarkers of CAD.

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Section: Resultsmentioning

confidence: 99%

KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS are promising novel biomarkers for diagnosis of coronary artery disease

Zhang

Wang

et al. 2019

Clin Exp Pharma Physio

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“…Long non-coding RNA Hox transcript antisense intergenic RNA (HOTAIR) was much lower in ECs and peripheral blood lymphocytes from atherosclerotic plaques in CAD patients (115). HOTAIR protected ECs against ox-LDL-induced apoptosis (115,116). In addition, HOTAIR was also significantly increased in ox-LDL-treated RAW264.7 cells and could reduce lipid accumulation and inhibit the inflammatory response by suppressing FXR1 via the NF-κB pathway (117).…”

Section: Hotairmentioning

confidence: 99%

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

Yan

Song

et al. 2020

Front. Immunol.

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Atherosclerosis is characterized as a chronic inflammatory response to cholesterol deposition in arteries. Low-density lipoprotein (LDL), especially the oxidized form (ox-LDL), plays a crucial role in the occurrence and development of atherosclerosis by inducing endothelial cell (EC) dysfunction, attracting monocyte-derived macrophages, and promoting chronic inflammation. However, the mechanisms linking cholesterol accumulation with inflammation in macrophage foam cells are poorly understood. Long non-coding RNAs (lncRNAs) are a group of non-protein-coding RNAs longer than 200 nucleotides and are found to regulate the progress of atherosclerosis. Recently, many lncRNAs interfering with cholesterol deposition or inflammation were identified, which might help elucidate their underlying molecular mechanism or be used as novel therapeutic targets. In this review, we summarize and highlight the role of lncRNAs linking cholesterol (mainly ox-LDL) accumulation with inflammation in macrophages during the process of atherosclerosis.

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“…Western Blot Analysis. Total proteins were isolated from cultured cells or freshly removed left ventricles as previously described [32]. Briefly, the myocardial homogenates or cell lysates were prepared in a RIPA lysis buffer with protease inhibitor cocktail (Roche), which were then subjected to scraping, sonication, and centrifugation.…”

Section: Determination On the Size Of Area At Risk (Aar) Andmentioning

confidence: 99%

The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury

Meng

Jiao

Zhu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA (Hotair) was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of Hotair were exposed to I/R surgery. H9c2 cells were cultured and subjected to hypoxia/reoxygenation (H/R) stimulation to further verify the role and underlying mechanisms of Hotair in vitro. Histological examination, molecular detection, and functional parameters were determined in vivo and in vitro. In response to I/R or H/R treatment, Hotair expression was increased in a bromodomain-containing protein 4-dependent manner. Cardiac-restricted knockdown of Hotair exacerbated, whereas Hotair overexpression prevented I/R-induced oxidative stress, cardiac myocyte apoptosis, and cardiac dysfunction. Mechanistically, we observed that Hotair exerted its beneficial effects via activating AMP-activated protein kinase alpha (AMPKα). Further detection revealed that Hotair activated AMPKα through regulating the enhancer of zeste homolog 2/microRNA-451/calcium-binding protein 39 (EZH2/miR-451/Cab39) axis. We provide the evidence that endogenous lncRNA Hotair is an essential negative regulator for oxidative stress and cardiac myocyte apoptosis in myocardial I/R injury, which is dependent on AMPKα activation via the EZH2/miR-451/Cab39 axis.

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Thymic stromal lymphopoietin-induced HOTAIR activation promotes endothelial cell proliferation and migration in atherosclerosis

Cited by 60 publications

References 28 publications

KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS are promising novel biomarkers for diagnosis of coronary artery disease

KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS are promising novel biomarkers for diagnosis of coronary artery disease

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury

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