Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p

Huang, Songqun; Tao, Wenqi; Guo, Zhian; Cao, Jiang; Huang, Xinmiao

doi:10.1016/j.gene.2019.02.098

Cited by 49 publications

(37 citation statements)

References 22 publications

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“…Long noncoding RNA GAS5 was proved to limit cell proliferation and fibrosis by sponging miR-221 and regulating SIRT1 levels in diabetic nephropathy [34]. Recently, a few lncRNAs including SOX2-OT were reported to be upregulated in MI [19,35]. Consistent with that, in our study, SOX2-OT presented higher level in HCMs induced by hypoxia relative to the control group.…”

Section: Discussionsupporting

confidence: 89%

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Yang

Lin

2020

Cardiovascular Therapeutics

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Background. Myocardial infarction (MI) was a severe cardiovascular disease resulted from acute, persistent hypoxia, or ischemia condition. Additionally, MI generally led to heart failure, even sudden death. A multitude of research studies proposed that long noncoding RNAs (lncRNAs) frequently participated in the regulation of heart diseases. The specific function and molecular mechanism of SOX2-OT in MI remained unclear. Aim of the Study. The current research was aimed to explore the role of SOX2-OT in MI. Methods. Bioinformatics analysis (DIANA tools and Targetscan) and a wide range of experiments (CCK-8, flow cytometry, RT-qPCR, luciferase reporter, RIP, caspase-3 activity, trans-well, and western blot assays) were adopted to investigate the function and mechanism of SOX2-OT. Results. We discovered that hypoxia treatment decreased cell viability but increased cell apoptosis. Besides, lncRNA SOX2-OT expression was upregulated in hypoxic HCMs. Hereafter, we confirmed that SOX2-OT could negatively regulate miR-27a-3p levels by directly binding with miR-27a-3p, and miR-27a-3p also could negatively regulate SOX2-OT levels. Furthermore, knockdown of SOX2-OT promoted cell proliferation, migration, and invasion, but limited cell apoptosis. However, these effects were reversed by anti-miR-27a-5p. Besides, we verified that miR-27a-3p binding with the 3′UTR of TGFBR1 and SOX2-OT regulated TGFβR1 level by collaborating with miR-27a-3p in HCMs. Eventually, rescue assays validated that the influence of SOX2-OT silence or miR-27a-3p overexpression on cellular processes in cardiomyocytes injury was counteracted by TGFBR1 overexpression. Conclusions. Long noncoding RNA SOX2-OT exacerbated hypoxia-induced cardiomyocytes injury by regulating miR-27a-3p/TGFβR1 axis, which may provide a novel insight for heart failure treatment.

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Section: Discussionsupporting

confidence: 89%

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Yang

Lin

2020

Cardiovascular Therapeutics

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“…Apoptosis has been reported to be induced under hypoxic stress in ischemic injury [21], and lncRNA UCA1 can regulate cardiomyocyte apoptosis in myocardial I/R injury [15]. LncRNA CARL is found to inhibit anoxia-induced cardiomyocyte apoptosis [22] and suppression of lncRNA TTTY15 can protect against hypoxia-induced cardiomyocyte apoptosis [23], suggesting the latent role of these lncRNAs in IMI. Currently, we investigated the possible impacts of lncRNA RP4 on the hypoxia-disposed damage in H9c2 cells.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

Rong

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Moreover, increased number of TUNEL‐positive cells declined upon HIF1A‐AS2 inhibition; however, HIF1A‐AS2 elevation promoted apoptosis in hypoxic HCMs (Figure 1F). In addition, the modulating function of RNAs in migration and invasion of HCMs has been investigated in some researches (Huang et al, 2019). Here, hypoxia inhibited cell migration and invasion of HCMs, then HIF1A‐AS2 overexpression or HIF1A‐AS2 knockdown aggravated or weakened hypoxia suppression‐mediated migration and invasion of HCMs (Figure S1A and B).…”

Section: Resultsmentioning

confidence: 99%

“…In MI, MALAT1 knockdown relieves acute MI via targeting miR‐320/Pten axis (Hu et al, 2018). Suppression of lncRNA TTTY15 weakens hypoxia‐induced cardiomyocytes injury by sponging miR‐455‐5p (Huang et al, 2019). LINC‐PINT stimulates the mitogen‐activated protein kinase pathway to aggravate acute MI by modulating miR‐208a‐3p (Zhu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of HIF1A‐AS2 suppresses TRIM44 to protect cardiomyocytes against hypoxia‐induced injury

Luo

Zhu

et al. 2020

Cell Biology International

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Myocardial infarction (MI) is a common cardiovascular disease characterized by an interruption of blood and oxygen supply to the heart, which results in gradual damage to the myocardial tissue and ultimately heart failure. The role of long non‐coding RNAs in the pathology of MI remains in its infancy, but has been implicated in MI and other heart conditions. For example, the expression of a non‐coding RNA hypoxia‐inducible factor 1α (HIF1A)‐antisense RNA 2 (HIF1A‐AS2) has previously been linked to coronary heart disease, however, whether HIF1A‐AS2 expression is also high in MI has not been addressed. Here, we report that HIF1A‐AS2 is upregulated in hypoxia‐treated human cardiomyocytes (HMCs) compared with normal cardiomyocytes, and that silenced HIF1A‐AS2 inhibited apoptosis and facilitated viability, migration, and invasion of HMCs. Our data suggested that in MI, HIF1A‐AS2 upregulation was associated with miR‐623, which promoted expression of tripartite motif containing 44 (TRIM44). Moreover, by upregulating TRIM44 we were able to remedy the HIF1A‐AS2 repression of apoptosis in HMCs. Thus, we conclude that cardiomyocytes can be protected against hypoxic‐treated injury by knockdown of HIF1A‐AS2, which suppresses TRIM44, and that HIF1A‐AS2 overexpression is a prognostic indicator of MI.

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Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p

Cited by 49 publications

References 22 publications

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

Knockdown of HIF1A‐AS2 suppresses TRIM44 to protect cardiomyocytes against hypoxia‐induced injury

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