Long noncoding RNA <i>TUG1</i> contributes to cerebral ischaemia/reperfusion injury by sponging mir‐145 to up‐regulate <i>AQP4</i> expression

Shan, Weifeng; Chen, Wei; Zhao, Xian; Pei, Aijie; Chen, Manli; Yu, Yang; Zheng, Yan‐Song; Zhu, Shengmei

doi:10.1111/jcmm.14712

Cited by 47 publications

(45 citation statements)

References 30 publications

(60 reference statements)

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“…TUG1 is increased during cardiac fibroblast‐myofibroblast transformation (FMT) and inhibition of TUG1 ameliorates FMT through sponging miR‐29c . TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging miR‐145 to up‐regulate AQP4 expression . Knockdown of TUG1 reduces hypoxia‐induced pulmonary smooth muscle cells proliferation and survival through sponging miR‐328.…”

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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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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“…Recently, miRNA or LncRNA was identified to regulate AQP4 to protect cerebral ischemic reperfusion injury [11, 12, 16, 33]. In the present study, we further explore that the protective effect of MALAT1 in cerebral ischemic reperfusion injury was related to AQP4 expression.…”

Section: Discussionmentioning

confidence: 66%

Inhibition of LncRNA MALAT1 Attenuates Cerebral Ischemic Reperfusion Injury via Regulating AQP4 Expression

et al. 2020

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Stroke is one of the leading causes of mortality and disability worldwide. Long noncoding RNAs (lncRNAs) including MALAT1 have been shown to have critical roles in cerebral ischemia reperfusion injury (CIRI). However, the underlying mechanism of MALAT1 in CIRI has not been elucidated. The present study aimed to investigate the function and potential regulatory mechanism of MALAT1 in cerebral ischemic reperfusion injury. We established the middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation/reoxygenation (OGD/RX) model in vivo and in vitro, and then Cell Counting Kit-8 (CCK-8), RT-qPCR, flow cytometry analysis, lactate dehydrogenase (LDH) analysis, and 2,3,5-triphenyltetrazolium chloride (TTC) staining were used to examine cell viability, MALAT1, aquaporin-4 (AQP4) expression, LDH release, and infarct volume, respectively. The level of AQP4 was remarkably upregulated in CIRI 24 h/48 h or OGD/RX 24 h/48 h compared with the sham group. Knockdown of AQP4 could alleviate OGD/RX-induced injury through enhancing cell viability and reducing LDH release and the rate of apoptotic cells. Furthermore, we found that MALAT1 was also increased in OGD/RX 24 h/48 h and silencing of MALAT1 could decrease AQP4. Inhibition of MALAT1 could also protect OGD/RX-induced injury, while the protective effect of MALAT1 siRNA on cerebral ischemic reperfusion was disappeared after transfection with AQP4 plasmid, indicating that MALAT1 may play a protective role in brain stroke through regulating AQP4. Taken together, our study provides evidence that MALAT1 is involved in ischemic stroke by inhibiting AQP4. Therefore, MALAT1 may serve as a potential target for therapeutic intervention in ischemic brain injury.

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“…LC3 and Becline-1 are speci c markers to monitor autophagy, and the amount of LC3-II is closely correlated with autophagosomes [31,32]. A study supported the notion that the upregulation of autophagy was associated with a 45% reduction in infarct size [33].TUG1 knockdown reduced the infarction area and cell apoptosis in MCAO model mice, thus effectively protecting against brain I/R injury [13]. Taken together, knockdown TUG1 could alleviate renal I/R injury by promoting autophagy.…”

Section: Discussionmentioning

confidence: 79%

Long non-coding RNA TUG1/microRNA-29/PTEN axis in ischemia-reperfusion in a rat model

Xu¹,

Huang²,

Lin³

et al. 2020

Preprint

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Objective: Long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is increased under ischemia. This study intended to identify the potential competing endogenous RNA network involving TUG1 in renal ischemia-reperfusion (I/R).Methods: A rat model of acute renal injury induced by I/R was established, and the differentially expressed genes were analyzed by microarray. The levels of blood urea nitrogen (BUN), serum creatine (SCr), methylenedioxyphetamine (MDA) and superoxide dismutase (SOD) in serum of rats were measured. HE staining evaluated the pathological damage of renal tissues, western blot analysis detect the levels of apoptosis- and autophagy-related proteins, immunofluorescence staining detected LC3 fluorescence intensity, and transmission electron microscope observed autophagosomes. Pull-down assay and dual luciferase reporter gene assay were used to verify the targeting relationship among TUG1, miR-29 and PTEN. The effects of TUG1 on biological behaviors of renal tubular cells were evaluated by simulating the acute renal injury induced by I/R in vitro.Results: In vivo, the levels of BUN, SCr and MDA in serum of I/R-treated rats were increased, SOD level and autophagosomes were reduced, tubule epithelial cells were necrotic, and TUG1 was upregulated in renal tissues of I/R-treated rats, which were reversed by TUG1 knockdown. Autophagy inhibition attenuated the protective effect of TUG1 knockdown on I/R-treated rats. TUG1 could competitively bind to miR-29 to promote PTEN expression. In vitro, low expression of TUG1 promoted proliferation and autophagy of renal tubular cells and inhibited apoptosis.Conclusion: TUG1 knockdown promotes autophagy and improves acute renal injury in I/R-treated rats by binding to miR-29 to silence PTEN.

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Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir‐145 to up‐regulate AQP4 expression

Cited by 47 publications

References 30 publications

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

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

Inhibition of LncRNA MALAT1 Attenuates Cerebral Ischemic Reperfusion Injury via Regulating AQP4 Expression

Long non-coding RNA TUG1/microRNA-29/PTEN axis in ischemia-reperfusion in a rat model

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