WITHDRAWN: Detection and analysis of apoptosis- and autophagy-related miRNAs of vascular endothelial cells in a mouse chronic intermittent hypoxia model

Liu, Kaixiong; Chen, Gongping; Lin, Pingli; Huang, Jian-Chai; Lin, Xi Zhang; Qi, Jia-Chao; Lin, Qi‐Chang

doi:10.1016/j.lfs.2016.08.005

Cited by 4 publications

(5 citation statements)

References 17 publications

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“…Moreover, the targeting relationship between HIF-1α and microRNA-135a (miR-135a) has also been revealed by previous evidence (7). It has been observed that CIH results in differential expression of microRNAs (miRNAs) that regulate genes related to apoptosis or autophagy (8). More importantly, miR-135a-3p mediates angiogenesis and tissue repair through modulation of the p38 pathway in endothelial cells (9).…”

Section: Original Articlementioning

confidence: 85%

Silencing of the long non-coding RNA MEG3 suppresses the apoptosis of aortic endothelial cells in mice with chronic intermittent hypoxia via downregulation of HIF-1α by competitively binding to microRNA-135a

Ding¹,

Huang²,

Wu³

et al. 2020

J Thorac Dis

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Background: Chronic intermittent hypoxia (CIH) involves substantial cortico-hippocampal injury, causing impairments of neurocognitive, respiratory, and cardiovascular functions. Long non-coding RNAs (lncRNAs) participate in CIH functions and development. Therefore, we explored the mechanisms involving lncRNA maternally expressed gene 3 (MEG3) regulating the aortic endothelial function of CIH mice via regulation of microRNA-135a (miR-135a) and the hypoxia-inducible factor (HIF)-1α. Methods: Expression of MEG3, miR-135a, and HIF-1α in CIH mice and CIH-treated cells was detected.Then, the apoptosis and proliferation of the aortic endothelial cells were examined to verify whether miR-135a and HIF-1α participated in CIH. Next, the interactions between MEG3, miR-135a, and HIF-1α were explored. Later, the effects of MEG3/miR-135a/HIF-1α on the expression of proliferation-and apoptosisrelated factors and aortic injury were investigated via gain-and loss-of function studies both in vivo and in vitro.Results: MEG3 and HIF-1α were highly expressed while miR-135a was poorly expressed in CIH mice and CIH-modeled cells. Moreover, miR-135a targeted HIF-1α to promote cell proliferation and inhibit apoptosis. MEG3 regulated HIF-1α expression by competitively binding to miR-135a. More importantly, we found that the silencing of MEG3/HIF-1α and the overexpression of miR-135a inhibited the apoptosis and injury of aortic endothelial cells while promoting cell proliferation in CIH mice. Conclusions: Altogether, silencing of MEG3 suppressed the aortic endothelial injury and cell apoptosis in CIH mice by downregulating HIF-1α through sponging miR-135a, providing evidence of a potential therapeutic target for CIH.

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Section: Original Articlementioning

confidence: 85%

Silencing of the long non-coding RNA MEG3 suppresses the apoptosis of aortic endothelial cells in mice with chronic intermittent hypoxia via downregulation of HIF-1α by competitively binding to microRNA-135a

Ding¹,

Huang²,

Wu³

et al. 2020

J Thorac Dis

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“…Mouse aortic endothelial cells were obtained as described previously [ 16 ]. Cells were maintained in RPMI 1640 medium (Gibco, Gaithersburg, MD, USA) supplemented with 10% fetal bovine serum (FBS).…”

Section: Methodsmentioning

confidence: 99%

“…Cells were grown under normoxic (21% O 2 ) or hypoxic (1% O 2 ) conditions at 37°C/5% CO 2 . To perform IH, cells were treated as described previously [ 16 ]. In the CIH group, cells were maintained at 37°C at 5% CO 2 in a chamber (Oxycycler model A42, Biospherix) in which O 2 levels were alternated between 21% for 5 min and 1% for 10 min, for a total of 64 cycles (18 h).…”

Section: Methodsmentioning

confidence: 99%

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Inhibition of microRNA-218 reduces HIF-1α by targeting on Robo1 in mice aortic endothelial cells under intermittent hypoxia

Liu

Chen

et al. 2017

Oncotarget

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ObjectiveTo investigate the effects of miR-218 on expression of hypoxia-inducible factors 1α (HIF-1α), vascular endothelial growth factor (VEGF) and cell apoptosis in normal mice aortic endothelial cells under intermittent hypoxia (IH) condition.MethodsAnti-miR-218 inhibitor, miR-negative control and miR-218 mimic were used to tranfect the cells in different groups under IH condition. Both RT-PCR and Western blot were used to determine the expressions of HIF-1α and VEGF. Akt, p-Akt and cell apoptosis related proteins bcl-2, bax and caspase-3 and roundabout 1 (Robo1) were measured using Western blot. Cell apoptosis was evaluated by flow cytometry. Statistical analysis was performed using SPSS 18.0.ResultsExpression of miR-218 was significantly up-regulated in the IH group and was significantly inhibited when cells were transfected with miR-218 inhibitor. Down regulation of miR-218 could reduce the expression of HIF-1α and VEGF under intermittent hypoxia condition. In cells transfected with miR-218 mimic, expression of HIF-1α and VEGF significantly increased compared with the control. However, when treated with LY294002, the expression of HIF-1α and VEGF both decreased. Apoptosis assay showed that down regulation of miR-218 could inhibit intermittent hypoxia induced cell apoptosis, decrease expression of caspase-3 and bax and increase expression of bcl-2 under intermittent hypoxia condition. At last, silencing Robo1 could significantly enhance the expression of HIF-1α under IH condition.ConclusionInhibition of miR-218 could reduce the expression of HIF-1α and protect against IH-induced apoptosis in mice aortic endothelial cells. The effects were associated with PI3K/AKT pathway and might through targeting of Robo1.

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“…In a mouse model of intermittent hypoxia, chronic intermittent hypopnea was shown to alter miRNA expression and the endothelium. [ 14 ] Thus, miRNA may play an important role in the development of OSA and AS. Its differential expression in OSA may therefore be a useful biomarker to diagnose the risk of AS in OSA patients.…”

Section: Introductionmentioning

confidence: 99%

MiR-664a-3p expression in patients with obstructive sleep apnea

Chen

Qin

et al. 2018

Medicine

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The early prediction of atherosclerosis (AS) is important in the management of obstructive sleep apnea patients (OSA). MicroRNA (miRNA) plays a vital role in the evolution of OSA and AS. Its differential expression may therefore serve as a diagnostic and prognostic biomarker of AS in OSA. The aim of this study was to identify specific serum miRNAs that could serve as a novel screening signature of AS in OSA patients. The specificity and sensitivity of these miRNAs in the early diagnosis of AS in OSA patients were then determined.The 128 participants in this study underwent maximum carotid intima-media thickness (CIMT) measurements and polysomnography and were divided into 4 groups: 27 healthy volunteers with normal max-CIMT, 31 healthy volunteers with increased max-CIMT, 35 OSA patients with normal max-CIMT, and 35 OSA patients with iCIMT. MiRNA was extracted from the 12 participants’ serum (3 participants each groups) and used to establish miRNA libraries for deep sequencing. A total of 116 participants were quantified by qRT- PCR. Correlations between differential expression of miRNAs and CIMT were assessed using the Spearman correlation coefficient. Our study was approved by the Ethics Committee of our hospital and was conducted in line with the Helsinki Declaration.MiR-664a-3p expression was quantified by qRT-PCR. Correlations between miR-664a-3p expression and CIMT were assessed using the Spearman correlation coefficient. The results showed that the miR-664a-3p was downregulated in the OSA, OSA with iCMIT, and nCIMT groups compared with the control group.The demonstrated potential of circulating miR-664a-3p as a noninvasive marker of AS in essential OSA patients should be confirmed in further studies.

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WITHDRAWN: Detection and analysis of apoptosis- and autophagy-related miRNAs of vascular endothelial cells in a mouse chronic intermittent hypoxia model

Cited by 4 publications

References 17 publications

Silencing of the long non-coding RNA MEG3 suppresses the apoptosis of aortic endothelial cells in mice with chronic intermittent hypoxia via downregulation of HIF-1α by competitively binding to microRNA-135a

Silencing of the long non-coding RNA MEG3 suppresses the apoptosis of aortic endothelial cells in mice with chronic intermittent hypoxia via downregulation of HIF-1α by competitively binding to microRNA-135a

Inhibition of microRNA-218 reduces HIF-1α by targeting on Robo1 in mice aortic endothelial cells under intermittent hypoxia

MiR-664a-3p expression in patients with obstructive sleep apnea

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