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Inhibition of miR-193a-3p protects human umbilical vein endothelial cells against intermittent hypoxia-induced endothelial injury by targeting FAIM2.

抑制 miR-193a-3p 通过靶向 faim2 保护人脐静脉内皮细胞对抗间歇性缺氧诱导的内皮损伤。

  • 影响因子:5.5150
  • DOI:10.18632/aging.102729
  • 作者列表:"Chen Q","Lin G","Huang J","Chen L","Liu Y","Huang J","Zhang S","Lin Q
  • 发表时间:2020-01-29
Abstract

OBJECTIVE:The functions and molecular regulatory mechanisms of miR-193a-3p in cardiac injury induced by obstructive sleep apnea (OSA) are poorly understood. This study aimed to explore the role of miR-193a-3p in intermittent hypoxia(IH)-induced human umbilical vein endothelial cells (HUVECs) injury. RESULTS:In this study, we found that IH significantly decreased viability but enhanced cell apoptosis. Concurrently, the miR-193a-3p expression level was increased in HUVECs after IH. Subsequent experiments showed that IH-induced injury was ameliorated through miR-193a-3p silence. Fas apoptotic inhibitory molecule 2 (FAIM2) was predicted by bioinformatics analysis and further identified as a direct target gene of miR-193a-3p. Interestingly, the effect of miR-193a-3p inhibition under IH could be reversed by down-regulating FAIM2 expression. CONCLUSION:In conclusion, our study first revealed that miR-193a-3p inhibition could protect HUVECs against intermittent hypoxia-induced damage by negatively regulating FAIM2. These findings could advance our understanding of the underlying mechanisms for OSA-related cardiac injury. METHODS:We exposed HUVECs to IH condition; the expression levels of miR-193a-3p were detected by RT-qPCR. Cell viability, and the expressions of apoptosis-associated proteins were examined via CCK-8, and western blotting, respectively. Target genes of miR-193a-3p were confirmed by dual-luciferase reporter assay.

摘要

目的: miR-193a-3p 在阻塞性睡眠呼吸暂停 (OSA) 所致心脏损伤中的作用及分子调控机制尚不清楚。本研究旨在探讨 miR-193a-3p 在间歇低氧 (IH) 诱导的人脐静脉内皮细胞 (HUVECs) 损伤中的作用。 结果: 在本研究中,我们发现 IH 显著降低细胞活力,但增强细胞凋亡。同时,IH 后 HUVECs 中 miR-193a-3p 表达水平升高。随后的实验表明,IH 诱导的损伤通过 miR-193a-3p 沉默得到改善。通过生物信息学分析预测 Fas 凋亡抑制分子 2 (FAIM2),并进一步确定为 miR-193a-3p 的直接靶基因。有趣的是,IH 下 miR-193a-3p 抑制的作用可以通过下调 FAIM2 的表达来逆转。 结论: 总之,我们的研究首次揭示了 miR-193a-3p 抑制可以通过负调节 faim2 来保护 HUVECs 免受间歇性缺氧诱导的损伤。这些发现可以促进我们对 OSA 相关心脏损伤潜在机制的理解。 方法: 我们将 HUVECs 暴露于 IH 条件下,通过 RT-qPCR 检测 miR-193a-3p 的表达水平。分别通过 CCK-8 和 western blotting 检测细胞活力和凋亡相关蛋白的表达。通过双荧光素酶报告基因检测确定 miR-193a-3p 的靶基因。

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相关文献
影响因子:5.5150
发表时间:2020-01-29
来源期刊:Aging
DOI:10.18632/aging.102729
作者列表:["Chen Q","Lin G","Huang J","Chen L","Liu Y","Huang J","Zhang S","Lin Q"]

METHODS:OBJECTIVE:The functions and molecular regulatory mechanisms of miR-193a-3p in cardiac injury induced by obstructive sleep apnea (OSA) are poorly understood. This study aimed to explore the role of miR-193a-3p in intermittent hypoxia(IH)-induced human umbilical vein endothelial cells (HUVECs) injury. RESULTS:In this study, we found that IH significantly decreased viability but enhanced cell apoptosis. Concurrently, the miR-193a-3p expression level was increased in HUVECs after IH. Subsequent experiments showed that IH-induced injury was ameliorated through miR-193a-3p silence. Fas apoptotic inhibitory molecule 2 (FAIM2) was predicted by bioinformatics analysis and further identified as a direct target gene of miR-193a-3p. Interestingly, the effect of miR-193a-3p inhibition under IH could be reversed by down-regulating FAIM2 expression. CONCLUSION:In conclusion, our study first revealed that miR-193a-3p inhibition could protect HUVECs against intermittent hypoxia-induced damage by negatively regulating FAIM2. These findings could advance our understanding of the underlying mechanisms for OSA-related cardiac injury. METHODS:We exposed HUVECs to IH condition; the expression levels of miR-193a-3p were detected by RT-qPCR. Cell viability, and the expressions of apoptosis-associated proteins were examined via CCK-8, and western blotting, respectively. Target genes of miR-193a-3p were confirmed by dual-luciferase reporter assay.

翻译标题与摘要 下载文献
影响因子:8.96
发表时间:2020-01-17
来源期刊:Circulation research
DOI:10.1161/CIRCRESAHA.119.315067
作者列表:["Du Y","Wang X","Li L","Hao W","Zhang H","Li Y","Qin Y","Nie S","Christopher TA","Lopez BL","Lau WB","Wang Y","Ma XL","Wei Y"]

METHODS:RATIONALE:Obstructive sleep apnea-hypopnea syndrome, a sleep breathing disorder in which chronic intermittent hypoxia (CIH) is the primary pathology, is associated with multiple cardiovascular diseases. However, whether and how CIH may affect cardiac remodeling following myocardial infarction (MI) remains unknown. OBJECTIVE:To determine whether CIH exposure at different periods of MI may exacerbate post-MI heart failure and to identify the mechanisms underlying CIH-exacerbated post-MI remodeling. METHODS AND RESULTS:Adult male mice were subjected to MI (4 weeks) with and without CIH (4 or 8 weeks). CIH before MI (CIH+MI) had no significant effect on post-MI remodeling. However, double CIH exposure (CIH+MI+CIH) or CIH only during the MI period (MI+CIH) significantly exacerbated pathological remodeling and reduced survival rate. Mechanistically, CIH activated TGF-β (tumor growth factor-β)/Smad (homologs of both the Drosophila protein MAD and the C. elegans protein SMA) signaling and enhanced cardiac epithelial to mesenchymal transition, markedly increasing post-MI cardiac fibrosis. Transcriptome analysis revealed that, among 15 genes significantly downregulated (MI+CIH versus MI), Ctrp9 (a novel cardioprotective cardiokine) was one of the most significantly inhibited genes. Real-time polymerase chain reaction/Western analysis confirmed that cardiomyocyte CTRP9 expression was significantly reduced in MI+CIH mice. RNA-sequencing, real-time polymerase chain reaction, and dual-luciferase reporter assays identified that microRNA-214-3p is a novel Ctrp9 targeting miRNA. Its upregulation is responsible for Ctrp9 gene suppression in MI+CIH. Finally, AAV9 (adeno-associated virus 9)-mediated cardiac-specific CTRP9 overexpression or rCTRP9 (recombinated CTRP9) administration inhibited TGF-β/Smad and Wnt/β-catenin pathways, attenuated interstitial fibrosis, improved cardiac function, and enhanced survival rate in MI+CIH animals. CONCLUSIONS:This study provides the first evidence that MI+CIH upregulates miR-214-3p, suppresses cardiac CTRP9 (C1q tumor necrosis factor-related protein-9) expression, and exacerbates cardiac remodeling, suggesting that CTRP9 may be a novel therapeutic target against pathological remodeling in MI patients with obstructive sleep apnea-hypopnea syndrome.

翻译标题与摘要 下载文献
影响因子:2.83
发表时间:2020-01-15
DOI:10.5664/jcsm.8124
作者列表:["Mendelson M","Inami T","Lyons O","Alshaer H","Marzolini S","Oh P","Bradley TD"]

METHODS:STUDY OBJECTIVES:Sleep apnea (SA) is prevalent among patients with coronary artery disease (CAD) and increases cardiovascular risk. A previous study showed that 1 month of cardiac rehabilitation (CR) reduced severity of SA in patients with CAD by reducing fluid accumulation in the legs during the day and the amount of fluid shifting rostrally into the neck overnight. The aim of this study was to evaluate whether CR will lead to longer-term attenuation of SA in patients with CAD. METHODS:Fifteen patients with CAD and SA who had participated in a 1-month randomized trial of the effects of exercise training on SA were followed up until they completed 6 months of CR (age: 65 ± 10 years; body mass index: 27.0 ± 3.9 kg/m²; apnea-hypopnea index [AHI]: 39.0 ± 16.7). The AHI was evaluated at baseline by polysomnography and then at 6 months by portable monitoring at home. Cardiorespiratory fitness (VO2peak) was evaluated via a graded cardiopulmonary exercise test at baseline and 6 months later. The 6-month CR program included once weekly, 90-minute, in-facility exercise sessions, and 4 days per week at-home exercise sessions. RESULTS:After 6 months of CR, there was a 54% reduction in the AHI (30.5 ± 15.2 to 14.1 ± 7.5, P < .001). Body mass index remained unchanged, but VO2peak increased by 27% (20.0 ± 6.1 to 26.0 ± 8.9 mL/kg/min, P = .04). CONCLUSIONS:Participation in CR is associated with a significant long-term decrease in the severity of SA. This finding suggests that attenuation of SA by exercise could be a mechanism underlying reduced mortality following participation in CR in patients with CAD and SA. CLINICAL TRIAL REGISTRATION:This study is registered at www.controlled-trials.com with identifier number ISRCTN50108373.

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