Up‐regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR‐182‐5p/IGF1 axis

Wang, Dong; Lin, Bin; Zhang, Wen

doi:10.1002/cbin.11333

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…The most important findings of our study were that, after we knocked down SNHG6 expression in HiPSC, the downregulation pattern of SNHG6 can be maintained until cardiac differentiation and we were able to show the rescuing effects of SNHG6 downregulation on PPFinduced cytotoxicity in HiPSC-CMs. Within the superfamily of SNHG lncRNAs, newly emerged evidence suggested that, other members than SNHG6, such as SNHG1 and SNHG16 are also actively involved in the development and pathology of cardiomyocytes (31,32). Our preliminary data also showed gene expression changes of other SNHG super-family than SNHG6 (data not shown).…”

Section: Discussionmentioning

confidence: 53%

Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes

Ren¹,

Hu²

2020

Cardiovasc Diagn Ther

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Background: Propofol (PPF) overdose is a rare but lethal condition, which may lead to severe cardiac failure. In this study, we established an in vitro PPF-induced cardiac cytotoxicity model, and investigate the functional role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6).Methods: Human induced pluripotent stem cell-derived cardiomyocytes (HiPSC-CMs) were exposed to PPF in vitro. PPF-induced cytotoxic effects were measured. PPF-induced SNHG6 expression change in HiPSC-CMs were monitored by qRT-PCR. SNHG6 was downregulated in HiPSC-CMs to examine its role in PPF-induced cardiac cytotoxicity. The expression of competing endogenous RNA (ceRNA) candidate of SNHG6, human microRNA-186-5p (hsa-miR-186-5p) was also investigated in PPF-exposed HiPSC-CMs. Functions of hsa-miR-186-5p were further investigated in PPF-exposed and SNHG6-downregulated HiPSC-CMs.Results: PPF induced significant cytotoxicity, as well as SNHG6 upregulation in HiPSC-CMs. SNHG6 downregulation had rescuing effects on PPF-induced cardiac cytotoxicity. Dual-luciferase activity assay confirmed that hsa-miR-186-5p was the ceRNA candidate of SNHG6. QRT-PCR showed hsa-miR-186-5p expression was reversely correlated with SNHG6 in PPF-exposed HiPSC-CMs. Suppressing hsa-miR-186-5p reduced the rescuing effects of SNHG6-downregulation on PPF-induced cardiac cytotoxicity.Conclusions: SNHG6/hsa-miR-186-5p can modulate PPF-induced cardiac cytotoxicity in HiPSC-CMs, and thus may be a future drug target to prevent PPF infusion syndrome.

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Section: Discussionmentioning

confidence: 53%

Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes

Ren¹,

Hu²

2020

Cardiovasc Diagn Ther

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“…miR-182-5p can prevent cardiac hypertrophy by regulating angiogenesis [ 32 , 33 ] and overexpressed miR-182-5p weakens the tube formation potential of vascular endothelial cells [ 34 ]. Our results revealed a similar expression pattern of miR-182-5p in the umbilical vein endothelial cells (HUVECs) and myocardial cells (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Mesenchymal stem cell-derived exosomal microRNA-182-5p alleviates myocardial ischemia/reperfusion injury by targeting GSDMD in mice

Yue

Luo

et al. 2022

Cell Death Discov.

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Recent evidence indicates that exosomes derived from mesenchymal stem cells (MSCs) confer protective effects against myocardial ischemia/reperfusion (I/R) injury. Exosomes are carriers of potentially protective endogenous molecules, including microRNAs (miRNAs/miRs). The current study set out to test the effects of transferring miR-182-5p from MSC-derived exosomes into myocardial cells on myocardial I/R injury. First, an I/R mouse model was developed by left anterior descending coronary artery occlusion, and myocardial cells were exposed to hypoxia/reoxygenation (H/R) for in vitro I/R model establishment. Loss- and gain-of-function experiments of miR-182-5p and GSDMD were conducted to explore the effects of miR-182-5p via MSC-derived exosomes on cell pyroptosis and viability. GSDMD was robustly expressed in I/R-injured myocardial tissues and H/R-exposed myocardial cells. GSDMD upregulation promoted H/R-induced myocardial cell pyroptosis and reduced viability, corresponding to increased lactate dehydrogenase release, reactive oxygen species production, and pyroptosis. A luciferase assay demonstrated GSDMD as a target of miR-182-5p. In addition, exosomal miR-182-5p was found to diminish GSDMD-dependent cell pyroptosis and inflammation induced by H/R. Furthermore, MSC-derived exosomes carrying miR-182-5p improved cardiac function and reduced myocardial infarction, accompanied with reduced inflammation and cell pyroptosis in vivo. Taken together, our findings suggest a cardioprotective effect of exosomal miR-182-5p against myocardial I/R injury, shedding light on an attractive therapeutic strategy.

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“…A previous study indicates that silenced SNHG16 represses Ang II-imposed cardiac hypertrophy ( 18 ). In the present study, SNHG16 was upregulated in myocardial I/R injury and inhibition of SNHG16 could significantly improve I/R damage.…”

Section: Discussionmentioning

confidence: 96%

Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

Geng

Xing

et al. 2023

Exp Ther Med

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Accumulating evidence shows that long non-coding RNAs (lncRNAs) are widely involved in cellular processes of myocardial ischemia/reperfusion (I/R). The present study investigated the functions of lncRNA SNHG16 in myocardial I/R and the mechanism mediated by SNHG16. The myocardial I/R rat and cell model and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established to detect the expression of SNHG16. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Myocardial cell apoptosis was assessed by TUNEL staining. Dual-luciferase gene reporter was applied to determine the interaction between the molecules. The expressions of SNHG16 were upregulated in myocardial I/R injury models. Inhibition of SNHG16 relieved myocardial I/R injury in vivo and in vitro silencing of SNHG16 alleviated H/R induced cardiomyocyte apoptosis. To explore the regulatory mechanism, it was discovered that SNHG16 directly interacted with miR-183, while forkhead box O1 (FoxO1) was a target of microRNA (miR)-183. Findings from rescue assays revealed that miR-183 inhibitor and upregulation of FOXO1 can rescue the effect of sh-SNHG16 on H/R-induced cardiomyocyte apoptosis. The results indicated that the lncRNA SNHG16/miR-183/FOXO1 axis exacerbated myocardial cell apoptosis in myocardial I/R injury, suggesting SNHG16 as a potential therapeutic target for myocardial I/R injury.

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Up‐regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR‐182‐5p/IGF1 axis

Cited by 12 publications

References 31 publications

Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes

Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes

Mesenchymal stem cell-derived exosomal microRNA-182-5p alleviates myocardial ischemia/reperfusion injury by targeting GSDMD in mice

Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

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