Long non‑coding RNA SENCR alleviates the inhibitory effects of rapamycin on human umbilical vein endothelial cells

Sun, Haitao; Wang, Shuiyun; Song, Min

doi:10.3892/mmr.2018.9094

Cited by 13 publications

(9 citation statements)

References 29 publications

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“…Recently, some lncRNAs have been identified in ECs treated with different stimuli, including TNF-α ( 37 ), serum deprivation ( 38 ), hypoxia ( 39 ) and rapamycin ( 40 ). These lncRNAs regulate the cell viability, proliferation, migration and angiogenesis of ECs by sponging miRNA-21 and miR-199a-5p, as well as by modulating VEGFR2, ERK1/2, respectively.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis

et al. 2021

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Endothelial dysfunction and diabetic vascular disease induced by chronic hyperglycemia involve complex interactions among high glucose, long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs) and the Ser/Thr kinase AKT. However, the molecular mechanisms under-lying the regulatory crosstalk between these have not yet been completely elucidated. Thus, the present study aimed to explore the molecular mechanisms whereby high glucose (HG)-induced lncRNA MIR181A2HG modulates human umbilical vein endothelial cell (HUVEC) proliferation and migration by regulating AKT2 expression. The persistent exposure of HUVECs to HG resulted in MIR181A2HG down-regulation and thus reduced its ability to sponge miR-6832-5p, miR-6842-5p and miR-8056, subsequently leading to an increase in miR-6832-5p, miR-6842-5p and miR-8056 levels. Mechanistically, miR-6832-5p, miR-6842-5p and miR-8056 were found to target the 3′UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2. Thus, this also led to the suppression of HUVEC proliferation and migration, and the formation of capillary-like structures. Moreover, the suppression of HUVEC proliferation and migration induced by MIR181A2HG downregulation was accompanied by changes in glucose metabolism. On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis. The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG-induced endothelial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis

et al. 2021

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“…Some risk factors have effects on transgenerational inheritance and epigenetic memory effects, highlighting the necessity of epigenetic drugs. (Boulberdaa, et al, 2016;H. Sun, Wang, & Song, 2018) SENCR Myocardin VSMC ↓Smooth muscle cell migration ↑Contractile phenotype (Bell, et al, 2014) STEEL KLF2, eNOS EC ↑Angiogenic microvessels (Man, et al, 2018) MALAT1 EC Mechanosensitive (Qiao, et al, 2016) MALAT1 Cell cycle regulators EC Hypoxia responsive ↑Angiogenesis (Michalik, et al, 2014; MALAT1 β-catenin/CD36 Mφ ↑Foam cell formation (Huangfu, et al, 2018) MALAT1 Mφ, splenocytes ↑ Atherosclerosis lesion in MALAT1 +/− ; ApoE −/− mice ↑ Immune system dysregulation ↓TNFa, iNOS (Gast, et al, (Berbee, et al, 2013;Fukao, et al, 2004;Hibender, et al, 2016;Howitz, et al, 2003;Norata, et al, 2007 Fry, et al, 2016) SRT2104 SIRT1 activator Cigarette Smokers Patients with T2DM…”

Section: Abca1mentioning

confidence: 99%

Targeting epigenetics and non-coding RNAs in atherosclerosis: from mechanisms to therapeutics

Kamato

Little

et al. 2019

Pharmacology & Therapeutics

127

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Atherosclerosis, the principal cause of cardiovascular death worldwide, is a pathological disease characterized by fibro-proliferation, chronic inflammation, lipid accumulation, and immune disorder in the vessel wall. As the atheromatous plaques develop into advanced stage, the vulnerable plaques are prone to rupture, which causes acute cardiovascular events, including ischemic stroke and myocardial infarction. Emerging evidence has suggested that atherosclerosis is also an epigenetic disease with the interplay of multiple epigenetic mechanisms. The epigenetic basis of atherosclerosis has transformed our knowledge of epigenetics from an important biological phenomenon to a burgeoning field of cardiovascular research. Here, we provide a systematic and up-to-date overview of the current knowledge of three distinct but interrelated epigenetic processes (including DNA methylation, histone methylation/acetylation, and noncoding RNAs), in atherosclerotic plaque development and instability. Mechanistic and conceptual advances in understanding the biological roles of various epigenetic modifiers in regulating gene expression and functions of endothelial cells (vascular homeostasis, leukocyte adhesion, endothelial-mesenchymal transition, angiogenesis, and mechanotransduction), smooth muscle

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“…Rapamycin inhibits cells without selectivity. It can prevent the growth of endothelial cells and smooth muscle cells simultaneously [38]. The inhibition mechanism is that rapamycin can combine with FK506 binding protein (FKBP) in cells, thus impeding the transition from the G1 to S stage [39].…”

Section: Resultsmentioning

confidence: 99%

Surface-Degradable Drug-Eluting Stent with Anticoagulation, Antiproliferation, and Endothelialization Functions

Hou

Wang

et al. 2019

Biomolecules

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Drug-eluting stents (DES) have been widely applied for saving the life of patients with coronary artery diseases (CADs). However, conventional polymers such as polylactic acid (PLA) and poly (lactic-co-glycolic acid) (PLGA), which are widely applied for drug-eluting stents studies, have serious bulk erosion problems, like high local acidity and poor mechanical properties. Instead, we chose surface erosion polymer poly (1, 3-trimethylene carbonate) (PTMC) as a drug carrier in this study. Here, we fabricated and characterized a novel durable-polymer drug-eluting 316 L stainless steel (SS) stent, in which the inner surface was coated with a Ti–O film using the magnetron sputtering method to promote the growth of endothelial cells (ECs). On the outer layer of the stent, first, a Ti–O film was deposited and, then, on top of it a rapamycin-loaded PTMC coat was deposited using the ultrasonic atomization spray method. This dual coating inhibited the migration and expansion of smooth muscle cells (SMCs). The drug coating also inhibited the adhesion/activation of platelets. In tests on dogs, it was found the novel stent promoted re-endothelialization and reduced restenosis, in contrast to the plain SS stent. Thus, the novel stent may have promise for use in treating patients with CAD.

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Long non‑coding RNA SENCR alleviates the inhibitory effects of rapamycin on human umbilical vein endothelial cells

Cited by 13 publications

References 29 publications

Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis

Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis

Targeting epigenetics and non-coding RNAs in atherosclerosis: from mechanisms to therapeutics

Surface-Degradable Drug-Eluting Stent with Anticoagulation, Antiproliferation, and Endothelialization Functions

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