Knockdown of lnc<scp>RNA AK</scp>139328 alleviates myocardial ischaemia/reperfusion injury in diabetic mice via modulating miR‐204‐3p and inhibiting autophagy

Yu, Siyang; Dong, Bin; Fang, Zhenfei; Hu, Xinqun; Tang, Liang; Zhou, Shenghua

doi:10.1111/jcmm.13754

Cited by 131 publications

(86 citation statements)

References 27 publications

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“…Excessive inhibition of Beclin1 markedly increases cardiomyocyte death in response to hypoxia/reoxygenation injury (Issa et al, 2018). However, it has also been reported that different mechanisms to inhibit autophagy also protect against myocardial ischemia/reperfusion injury (Wu et al, 2018;Yu et al, 2018). It has been found that application of 3-MA to inhibit autophagy alleviates astrocyte injury by inhibiting LMP (Zhou et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

The Lysosomal Membrane Protein Lamp2 Alleviates Lysosomal Cell Death by Promoting Autophagic Flux in Ischemic Cardiomyocytes

Cui

Zhao

et al. 2020

Front. Cell Dev. Biol.

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Lysosomal membrane permeabilization (LMP) has recently been recognized as an important cell death pathway in various cell types. However, studies regarding the correlation between LMP and cardiomyocyte death are scarce. Lysosomal membraneassociated protein 2 (Lamp2) is an important component of lysosomal membranes and is involved in both autophagy and LMP. In the present study, we found that the protein content of Lamp2 gradually decreased in response to oxygen, glucose and serum deprivation (OGD) treatment in vitro. To further elucidate its role in ischemic cardiomyocytes, particularly with respect to autophagy and LMP, we infected cardiomyocytes with adenovirus carrying full-length Lamp2 to restore its protein level in cells. We found that OGD treatment resulted in the occurrence of LMP and a decline in the viability of cardiomyocytes, which were remarkably reversed by Lamp2 restoration. Exogenous expression of Lamp2 also significantly alleviated the autophagic flux blockade induced by OGD treatment by promoting the trafficking of cathepsin B (Cat B) and cathepsin D (Cat D). Through drug intervention and gene regulation to alleviate and exacerbate autophagic flux blockade respectively, we found that impaired autophagic flux in response to ischemic injury contributed to the occurrence of LMP in cardiomyocytes. In conclusion, our present data suggest that Lamp2 overexpression can improve autophagic flux blockade probably by promoting the trafficking of cathepsins and consequently conferring cardiomyocyte resistance against lysosomal cell death (LCD) that is induced by ischemic injury. These results may indicate a new therapeutic target for ischemic heart damage.

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Section: Discussionmentioning

confidence: 99%

The Lysosomal Membrane Protein Lamp2 Alleviates Lysosomal Cell Death by Promoting Autophagic Flux in Ischemic Cardiomyocytes

Cui

Zhao

et al. 2020

Front. Cell Dev. Biol.

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“…In a recent study, Yu et al [35] showed that silencing lncRNA AK139328 signi cantly increased miR-204-3p expression and inhibited autophagy of cardiomyocyte, thereby reducing myocardial ischemia/reperfusion injury (MIRI) in diabetic mice. Comparably, Xiao et al [36] discovered that ischemiareperfusion (IR) could down-regulate miR-204, while up-regulated the proportion of LC3-II protein and autophagy cell.…”

Section: Mirna-204 May Play a Critical Role In Cardiovascular Diseasesmentioning

confidence: 99%

Serum microRNA-204 Levels are Associated with Long-Term Cardiovascular Diseases Risk Using Framingham Risk Score in Patients with Type 2 Diabetes: Results From an Observational Study

Wang

Ding

Pei

et al. 2020

Preprint

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Background: The basic studies have demonstrated that microRNA-204 (miRNA-204) was involved in the process of atherosclerosis and vascular calcification. However, the value of miRNA-204 as a predictive biomarker for cardiovascular disease (CVD) is still controversial. The purpose of the present study was to evaluate the association between circulating miRNA-204 level and the 10-year cardiovascular disease risk score, Framingham risk score (FRS).Method: The subjects consecutively enrolled 194 patients with type 2 diabetes mellitus without cardiovascular disease at Anzhen Hospital from January 2015 to September 2016. We used the Framingham Risk Score (FRS) to evaluate the risk of cardiovascular disease. Circulating miRNA-204 levels were measured by quantitative Real-Time polymerase chain reaction (qRT-PCR).Result: The circulating miRNA-204 levels were significantly lower in high risk group of CVD (FRS > 20%) of patients (0.49 ± 0.13) compared with that in low risk group (FRS < 10%) and intermediate risk group (FRS = 10%-20%) (0.87 ± 0.19, 0.75 ± 0.25, Respectively, p < 0.001). FRS was negatively correlated with miR-204 levels (r=-0.421, p < 0.001). According to multivariate logistic analyses, miRNA-204 levels were still significantly and independently associated with the high risk of CVD after adjusting the conventional risk factor. Receiver-operating characteristic curve (ROC) analysis also showed that circulating miRNA-204 level can predict the high risk of CVD, and the specificity was higher than traditional risk factors SBP and protective factor HDL-C of CVD.Conclusion: Our study demonstrated that patients with lower circulating miRNA-204 levels were at a high risk for the progression of CVD. After adjustment for potential confounders, miRNA-204 was independently associated with CVD in patients with T2DM.

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“…For instance, L. H. Liu, Yue, et al (2016) Recently, researchers suggested that lncRNAs may regulate gene expression and tumor progression through regulating miRNA expression (Li, Hu, et al, 2016;. For instances, S. Yu et al (2018) indicated that knockdown of lncRNA AK139328 alleviated myocardial reperfusion/ischemia injury through regulating miR-204-3p and suppressing autophagy. Jiang et al (2018) showed that lncRNA TPT1-AS1 induced cell proliferation and metastasis through playing as a sponge of miR-324-5p in cervical cancer.…”

Section: The Expression Of Mir-214-3p Was Increased In the Bladdermentioning

confidence: 99%

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

Wang

Zhu

et al. 2019

Journal Cellular Physiology

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Growing evidence suggested that the long noncoding RNAs (lncRNAs) regulate several pathophysiological processes in tumorigenesis and may be new biomarkers for tumor therapy. In this study, we studied the expression and role of lncRNA MT1JP in the development of bladder cancer. We demonstrated that the expression of MT1JP was downregulated in bladder tumor samples and cell lines. Ectopic expression of MT1JP suppressed cell proliferation, cycle, and invasion in bladder cancer. In addition, our result suggested that miR‐214‐3p overexpression decreased the luciferase activity of wild‐type MT1JP but not mutated‐type MT1JP and elevated expression of MT1JP decreased miR‐214‐3p expression in the bladder cancer cell. Furthermore, we indicated that the expression of miR‐214‐3p was upregulated in bladder tumor samples and cell lines. Ectopic expression of miR‐214‐3p promoted cell proliferation, cycle, and invasion in bladder cancer. MT1JP suppressed cell proliferation, cycle, and invasion via negative modulation of miR‐214‐3p in bladder cancer. These data suggested that lncRNA MT1JP acts a tumor suppressor gene in bladder cancer progression, considering MT1JP as a new therapeutic target in bladder cancer.

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

Cited by 131 publications

References 27 publications

The Lysosomal Membrane Protein Lamp2 Alleviates Lysosomal Cell Death by Promoting Autophagic Flux in Ischemic Cardiomyocytes

The Lysosomal Membrane Protein Lamp2 Alleviates Lysosomal Cell Death by Promoting Autophagic Flux in Ischemic Cardiomyocytes

Serum microRNA-204 Levels are Associated with Long-Term Cardiovascular Diseases Risk Using Framingham Risk Score in Patients with Type 2 Diabetes: Results From an Observational Study

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

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