Down-regulation of lncRNA KCNQ1OT1 protects against myocardial ischemia/reperfusion injury following acute myocardial infarction

Li, Xin; Dai, Yue; Yan, Shujun; Shi, Yanli; Han, Baihe; Li, Jingxiu; Cha, Li; Mu, Jianjun

doi:10.1016/j.bbrc.2017.08.005

Cited by 132 publications

(76 citation statements)

References 23 publications

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“…Previous researches have suggested that some lncRNAs were closely associated with myocardial ischaemia‐reperfusion. Li et al provide evidence for lncRNA KCNQ1OT1 knockdown being a preventive solution to MIRI 7. Zhao et al demonstrated that lncRNA MALAT1 was involved in myocardial ischaemia‐reperfusion and down‐regulation of MALAT1 contributed to the reduction of cardiomyocyte apoptosis 8.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA AK139328 alleviates myocardial ischaemia/reperfusion injury in diabetic mice via modulating miR‐204‐3p and inhibiting autophagy

Dong

Fang

et al. 2018

J Cellular Molecular Medi

131

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This study was aimed at investigating the effects of lncRNA AK139328 on myocardial ischaemia/reperfusion injury (MIRI) in diabetic mice. Ischaemia/reperfusion (I/R) model was constructed in normal mice (NM) and diabetic mice (DM). Microarray analysis was utilized to identify lncRNA AK139328 overexpressed in DM after myocardial ischaemia/reperfusion (MI/R). RT‐qPCR assay was utilized to investigate the expressions of lncRNA AK139328 and miR‐204‐3p in cardiomyocyte and tissues. Left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF) and fractioning shortening (FS) were obtained by transthoracic echocardiography. Haematoxylin‐eosin (HE) staining and Masson staining were utilized to detect the damage of myocardial tissues degradation of myocardial fibres and integrity of myocardial collagen fibres. Evans Blue/TTC staining was used to determine the myocardial infarct size. TUNEL staining was utilized to investigate cardiomyocyte apoptosis. The targeted relationship between lncRNA AK139328 and miR‐204‐3p was confirmed by dual‐luciferase reporter gene assay. MTT assay was used for analysis of cardiomyocyte proliferation. Western blot was utilized to investigate the expression of alpha smooth muscle actin (α‐SMA), Atg7, Atg5, LC3‐II/LC3‐I and p62 marking autophagy. Knockdown of lncRNA AK139328 relieved myocardial ischaemia/reperfusion injury in DM and inhibited cardiomyocyte autophagy as well as apoptosis of DM. LncRNA AK139328 modulated miR‐204‐3p directly. MiR‐204‐3p and knockdown of lncRNA AK139328 relieved hypoxia/reoxygenation injury via inhibiting cardiomyocyte autophagy. Silencing lncRNA AK139328 significantly increased miR‐204‐3p expression and inhibited cardiomyocyte autophagy, thereby attenuating MIRI in DM.

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Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA AK139328 alleviates myocardial ischaemia/reperfusion injury in diabetic mice via modulating miR‐204‐3p and inhibiting autophagy

Dong

Fang

et al. 2018

J Cellular Molecular Medi

131

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“…Recently, plenty of studies showed lncRNAs play critical roles in MI progression. For example, Li et al showed that lncRNA KCNQ1OT1 suppression protected against myocardial ischemia following acute MI [16]. Liu et al showed that lncRNA CAIF suppressed autophagy and attenuated MI through blocking p53-mediated myocardin transcription [17].…”

Section: Discussionmentioning

confidence: 99%

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

2019

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This study is aimed to explore the roles of LINC00528 in myocardial infarction (MI) progression. Quantitative real-time PCR showed that the expression of LINC00528 and COX-2 was upregulated while miR-143-3p expression was down-regulated in post-MI cells. In function assays, LINC00528 suppression promoted post-MI cells proliferation and reduced cell apoptosis in vitro. In mechanism, LINC00528 interacted with miR-143-3p in post-MI cells. COX-2 served as a target of miR-143-3p in post-MI cells. Besides, LINC00528 inhibition on COX-2 expression and post-MI cells progression could be partially abolished by miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI patients treatment. ARTICLE HISTORY

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“…Kcnq1ot1 has been reported to be associated with many disorders, particularly those related to heart disease [14][15][16][17]. Li et al [14] indicated that suppression of Kcnq1ot1 might prevent myocardial I/R injury following acute myocardial infarction via regulating AdipoR1. Jiang et al [15] elucidated that silencing Kcnq1ot1 could regulate QT interval prolongation via inhibiting Kcnq1 gene expression.…”

Section: Introductionmentioning

confidence: 99%

“…The lncRNA Kcnq1ot1, the full name of which is KCNQ1 overlapping transcript 1, is located in the KCNQ1 locus at 11p15.5 [13]. Kcnq1ot1 has been reported to be associated with many disorders, particularly those related to heart disease [14][15][16][17]. Li et al [14] indicated that suppression of Kcnq1ot1 might prevent myocardial I/R injury following acute myocardial infarction via regulating AdipoR1.…”

Section: Introductionmentioning

confidence: 99%

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

Yang

Qin

Wang

et al. 2018

Cell Physiol Biochem

146

109

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Background/Aims: Diabetic cardiomyopathy (DCM) is a common complication of diabetes and can cause heart failure, arrhythmia and sudden death. The pathogenesis of DCM includes altered metabolism, mitochondrial dysfunction, oxidative stress, inflammation, cell death and extracellular matrix remodeling. Recently, pyroptosis, a type of programmed cell death related to inflammation, was proven to be activated in DCM. However, the molecular mechanisms underlying pyroptosis in DCM remain elusive. The long non-coding RNA (lncRNA) Kcnq1ot1 participates in many cardiovascular diseases. This study aims to clarify whether Kcnq1ot1 affects cardiac pyroptosis in DCM. Methods: AC16 cells and primary cardiomyocytes were incubated with 5.5 and 50 mmol/L glucose. Diabetic mice were induced with streptozotocin (STZ). Kcnq1ot1 was silenced both in vitro and in vivo. qRT-PCR was used to detect the expression level of Kcnq1ot1. Immunofluorescence, qRT-PCR and western blot analyses were used to detect the degree of pyroptosis. Echocardiography, hematoxylin and eosin staining, and Masson’s trichrome staining were used to detect the cardiac function and morphology in mice. Cell death and function were detected using TUNEL staining, immunofluorescence staining and Ca²⁺ measurements. Results: The expression of Kcnq1ot1 was increased in patients with diabetes, high glucose-induced cardiomyocytes and diabetic mouse cardiac tissue. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1. Furthermore, silencing Kcnq1ot1 reduced cell death, cytoskeletal structure abnormalities and calcium overload in vitro and improved cardiac function and morphology in vivo. Conclusion: Kcnq1ot1 is overexpressed in DCM, and silencing Kcnq1ot1 inhibits pyroptosis by influencing miR-214-3p and caspase-1 expression. We clarified for the first time that Kcnq1ot1 could be a new therapeutic target for DCM.

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Down-regulation of lncRNA KCNQ1OT1 protects against myocardial ischemia/reperfusion injury following acute myocardial infarction

Cited by 132 publications

References 23 publications

Knockdown of lncRNA AK139328 alleviates myocardial ischaemia/reperfusion injury in diabetic mice via modulating miR‐204‐3p and inhibiting autophagy

Knockdown of lncRNA AK139328 alleviates myocardial ischaemia/reperfusion injury in diabetic mice via modulating miR‐204‐3p and inhibiting autophagy

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

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