Identification and analysis of a key long non‐coding RNAs (lncRNAs)‐associated module reveal functional lncRNAs in cardiac hypertrophy

Zhang, Jian; Feng, Chenchen; Song, Chao; Ai, Bo; Bai, Xuefeng; Liu, Yuejuan; Li, Xuecang; Zhao, Jian; Shi, Shengshu; Chen, Xin; Su, Xiaojie; Li, Chunquan

doi:10.1111/jcmm.13376

Cited by 15 publications

(12 citation statements)

References 46 publications

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“…Not much is known about gm26902 , except that its expression characterizes a subset of microglia CD11c+ population, which sustains brain development [ 31 ], while expression of gm17501 has been associated with cardiac hypertrophy [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Non-Coding Transcript Heterogeneity in Mesothelioma: Insights from Asbestos-Exposed Mice

Felley‐Bosco

Rehrauer

2018

IJMS

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Mesothelioma is an aggressive, rapidly fatal cancer and a better understanding of its molecular heterogeneity may help with making more efficient therapeutic strategies. Non-coding RNAs represent a larger part of the transcriptome but their contribution to diseases is not fully understood yet. We used recently obtained RNA-seq data from asbestos-exposed mice and performed data mining of publicly available datasets in order to evaluate how non-coding RNA contribute to mesothelioma heterogeneity. Nine non-coding RNAs are specifically elevated in mesothelioma tumors and contribute to human mesothelioma heterogeneity. Because some of them have known oncogenic properties, this study supports the concept of non-coding RNAs as cancer progenitor genes.

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Section: Discussionmentioning

confidence: 99%

Non-Coding Transcript Heterogeneity in Mesothelioma: Insights from Asbestos-Exposed Mice

Felley‐Bosco

Rehrauer

2018

IJMS

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“…LncRNAs usually exert their functions via recruiting specific RNA‐binding proteins, promoting target gene expression, influencing angiogenesis and by functioning as a competing endogenous RNA (ceRNA) . Whole‐genome transcriptome analysis showed that many cardiac‐specific lncRNAs play critical regulating roles in hypertrophic response and cardiac remodelling, indicating that lncRNAs may be the significant biological markers and therapeutic targets for cardiac hypertrophy …”

Section: Introductionmentioning

confidence: 99%

LncRNA TUG1 alleviates cardiac hypertrophy by targeting miR‐34a/DKK1/Wnt‐β‐catenin signalling

Fang

Liu

et al. 2020

J Cellular Molecular Medi

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Cardiac hypertrophy, classified as physiological and pathological hypertrophy, is an adaptive response of the heart to keep normal cardiac function in the condition of pathological injury or abnormal stress. 1 Physiological cardiac hypertrophy, caused by pregnancy or sports training, has normal morphological characteristics and helpful influences on the heart. 2 Pathological cardiac hypertrophy, accompanied by maladaptive cardiac remodelling, altered cardiac morphology as well as abnormal cardiac gene expressions, is the key induction factor for heart failure progression. 3 Although many factors have been confirmed to induce cardiac hypertrophy, 4 the underlying molecular mechanisms have not been stated clearly. LncRNAs, a series of highly conserved non-coding RNAs, are composed of more than 200 nucleotides. 5,6 With continuous advances in sequencing technology and large-scale genome sequencing projects, Abstract The current study was designed to explore the role and underlying mechanism of lncRNA taurine up-regulated gene 1 (TUG1) in cardiac hypertrophy. Mice were treated by transverse aortic constriction (TAC) surgery to induce cardiac hypertrophy, and cardiomyocytes were treated by phenylephrine (PE) to induce hypertrophic phenotype. Haematoxylin-eosin (HE), wheat germ agglutinin (WGA) and immunofluorescence (IF) were used to examine morphological alterations. Real-time PCR, Western blots and IF staining were used to detect the expression of RNAs and proteins. Luciferase assay and RNA pull-down assay were used to verify the interaction. It is revealed that TUG1 was up-regulated in the hearts of mice treated by TAC surgery and in PE-induced cardiomyocytes. Functionally, overexpression of TUG1 alleviated cardiac hypertrophy both in vivo and in vitro. Mechanically, TUG1 sponged and sequestered miR-34a to increase the Dickkopf 1 (DKK1) level, which eventually inhibited the activation of Wnt/β-catenin signalling.In conclusion, the current study reported the protective role and regulatory mechanism of TUG1 in cardiac hypertrophy and suggested that TUG1 may serve as a novel molecular target for treating cardiac hypertrophy. K E Y W O R D Scardiac hypertrophy, DKK 1, lncRNA TUG1, miR-34a, Wnt/β-catenin signalling

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“…A wholetranscriptome analysis of heart biopsy specimens from patients with DCM and healthy heart donors confirmed that myocardial infarction associated transcript was highly expressed in patients with DCM (23). To date, many lncRNAs have been revealed to be associated with myocardial pathophysiology, and research on the biological function and mechanism of lncRNAs has only begun and remained unclear (24,25). LncRNA X inactive-specific transcript (XIST) is indispensable for transcriptional silencing of the X chromosome in female mammals, which play vital role in the inactivation of the X chromosome (26).…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed long non-coding RNAs associated with dilated cardiomyopathy using integrated bioinformatics approaches

Luo

Zhang

2020

DD&T

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long Non-coding RNAs, biomarker, dilated cardiomyopathy, bioinformatics analysis The aim of this study was to identify novel long non-coding RNA (lncRNA) biomarkers associated with dilated cardiomyopathy (DCM) and reveal the potential molecular mechanisms of DCM development using bioinformatics approaches. The array data of GSE5406, including 108 DCM samples and 16 non-failing control samples, were obtained from the Gene Expression Omnibus database. The differentially expressed lncRNAs were identified using limma package in R. Pearson's correlation analyses were performed between the differentially expressed lncRNAs and protein-coding genes based on their expression levels. Pathway enrichment of these lncRNAs was conducted based on the significantly co-expressed genes. From the receiver operating characteristic (ROC) curve, the area under the ROC curve (AUC) value was obtained and used for evaluating discriminatory ability. IDI2-AS1 and XIST were differentially expressed in DCM patients. A total of 510 co-expressed genes were identified. The enriched functions and pathways of the co-expressed genes mainly included NADH dehydrogenase activity, cardiac muscle contraction, and oxidative phosphorylation. The ROC curve analysis indicated that the two lncRNAs have favorable diagnostic values in DCM. The AUC values of XIST, IDI2-AS1, and the combination of XIST and IDI2-AS1 were 0.733 (95% CI: 0.646-0.809), 0.796 (95% CI: 0.715-0.863), and 0.823 (95% CI: 0.745-0.886), respectively. This study identified IDI2-AS1 and XIST lncRNAs and related pathways involved in the pathogenesis of DCM, thus providing potential diagnostic and therapeutic targets for DCM.

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Identification and analysis of a key long non‐coding RNAs (lncRNAs)‐associated module reveal functional lncRNAs in cardiac hypertrophy

Cited by 15 publications

References 46 publications

Non-Coding Transcript Heterogeneity in Mesothelioma: Insights from Asbestos-Exposed Mice

Non-Coding Transcript Heterogeneity in Mesothelioma: Insights from Asbestos-Exposed Mice

LncRNA TUG1 alleviates cardiac hypertrophy by targeting miR‐34a/DKK1/Wnt‐β‐catenin signalling

Identification of differentially expressed long non-coding RNAs associated with dilated cardiomyopathy using integrated bioinformatics approaches

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