MicroRNA-200a/200b Modulate High Glucose-Induced Endothelial Inflammation by Targeting O-linked N-Acetylglucosamine Transferase Expression

Lo, Wan-Yu; Yang, Wenkai; Peng, Ching‐Tien; Pai, Wan-Yu

doi:10.3389/fphys.2018.00355

Cited by 42 publications

(44 citation statements)

References 43 publications

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“…However, there are other examples of miRNAs which are either downregulated (e.g., mir-29b, miR-200a/b) or upregulated (e.g., miR-155, mir-92a, miR-137) upon hyperglycemic/diabetic milieu in endothelial cells and contributing to endothelial inflammation and/or OxS deterioration. Specifically, these miRNAs were found to regulate redox balance via eNOS (miR-155), AMPKα1 (miR-137), O -GlcNAc transferase (OGT) (miR-200a/b) or components of Keap/Nrf2/HO-1 pathway (miR-92a, miR-200a) [ 245 , 246 , 247 , 248 , 249 , 250 ]. Interestingly, OxS was augmented due to lack of miR-29b-dependent regulation of AKT/eNOS signal pathway, as miR-29b was sponged by lncRNA H19 in vascular endothelium [ 245 ].…”

Section: Overview Of Mirnas—the Focus On Interplay With Oxidative mentioning

confidence: 99%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

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Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.

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Section: Overview Of Mirnas—the Focus On Interplay With Oxidative mentioning

confidence: 99%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

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“…MiR-223 increased the inflammation response via inhibitor of nuclear factor kappa-B (IκB) kinase α (IKKα) and mitogen-activated protein kinase phosphatase-5 (MKP-5) [ 7 ], whereas miR-200b suppressed tumor necrosis factor-α (TNF-α) induced interleukin-8 (IL-8) secretion and tight junction disruption of intestinal epithelial cells [ 8 ]. miR-200a/200b inhibited high-glucose induced endothelial inflammation by regulating O -GlicNAc transferase-mediated protein O-GlcNAcylation [ 9 ]. miR-200b/c attenuated lipopolysaccharide-induced early pulmonary fibrosis by targeting Zinc-finger E-box-binding homeobox 1/2 (ZEB1/2) via p38 mitogen-activated protein kinase (MAPK) and transforming growth factor-β (TGF-β)/smad3 signaling pathways [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-200b attenuates IL-6 production through IKKβ and ZEB1 in human gingival fibroblasts

et al. 2018

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ObjectiveMicroRNAs (miRNAs) play important roles in biological processes such as cell differentiation, development, infection, immune response, inflammation and tumorigenesis. We previously reported that the expression of miR-200b was significantly increased in inflamed gingiva compared with non-inflamed gingiva. To elucidate the roles of miR-200b in the inflamed gingiva, we have analyzed the effects of miR-200b on the expression of IL-6 in human gingival fibroblasts (HGF).Materials and methodsTotal RNA and protein were extracted from HGF after stimulation by interleukin-1β (IL-1β; 1 ng/ml) or tumor necrosis factor-α (TNF-α; 10 ng/ml) and transfected with miR-200b expression plasmid or miR-200b inhibitor. IL-6, IL-1β, inhibitor of nuclear factor kappa-B kinaseβ (IKKβ), Zinc-finger E-box-binding homeobox 1 (ZEB1) and E-cadherin mRNA and protein levels were analyzed by real-time PCR and Western blot.ResultsIL-1β and TNF-α increased IL-6 mRNA and protein levels, and they were significantly suppressed by miR-200b overexpression, whereas they were further increased by miR-200b inhibitor in HGF. IKKβ and ZEB1 which are target genes of miR-200b negatively regulate E-cadherin. MiR-200b suppressed the expression of IKKβ and ZEB1 and increased E-cadherin mRNA and protein levels in HGF.ConclusionsThese results suggest that miR-200b attenuates inflammatory response via IKKβ and ZEB1 in periodontal tissue.

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“…Next, interesting miRNA found in the present study is miR-146, alterations of which are associated with immune system response or with prolonged exercise [31,38], but there have been no reports so far about association of this miRNA with stress. In turn, miR-200 was sensitive to oxidative stress and modulated endothelial inflammation [39], but also regulated glucose levels in diabetes [40]. It could be suggested that expression alteration of miR-200 in the serum of NET-KO and SWR/J mice under stress conditions could be linked with alterations in the blood level of glucose.…”

Section: Discussionmentioning

confidence: 99%

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

Solich

Kuśmider

Faron-Górecka

et al. 2020

Cells

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In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and SWR/J. The procedure of restraint stress (RS, 4 h) was applied, and the following behavioral experiments (the forced swim test and sucrose preference test) indicated that NET-KO and SWR/J mice were less sensitive to RS than WT mice. Then, we aimed to find the miRNAs which changed in similar ways in the serum of NET-KO and SWR/J mice subjected to RS, being at the same time different from the miRNAs found in the serum of WT mice. Using Custom TaqMan Array MicroRNA Cards, with primers for majority of miRNAs expressed in the serum (based on a preliminary experiment using the TaqMan Array Rodent MicroRNA A + B Cards Set v3.0, Thermo Fisher Scientific, Waltham, MA, USA) allowed the identification of 21 such miRNAs. Our further analysis focused on miR-1 and miR-155 and their targets-these two miRNAs are involved in the regulation of BDNF expression and can be regarded as biomarkers of stress-resilience.Cells 2020, 9, 917 2 of 17 are regarded as endogenous "hubs" (as Issler and Chen have put it) for the fine tuning of target gene expression or an "expression switch", and can provide deeper insight into complex biological processes underlying stress response.In the present study, we used three strains of mice differentially reacting to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype [7-9], as well as two other strains of mice displaying different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and swiss SWR/J, described extensively by Szklarczyk and co-workers [10]. The different reaction to stress of these strains of mice has been confirmed by measuring corticosterone level. The NET-KO mice display a slower increase in corticosterone level after stress compared with WT animals, while corticosterone level was not changed at 2 h after restraint stress in the blood of SWR/J mice [8,10]. We applied the procedure of restraint stress (RS), which has been shown to induce an uncontrollable aversive situation that produces both physical and psychological consequences leading to neuronal and behavioral alterations [11]. The aim of following molecular studies was to find biomarkers for different behavioral responses to RS among miRNAs expressed in the serum of three genotypes under study. This goal was achieved, as we were able to identify a group of miRNAs differentiating the stress response of NET-KO and SWR/J mice from WT animals. The most interesting were the alterations in the miR-1 and miR-155 levels, which are involved in regulation of BDNF expression, which in turn affects important biochemical processes. Materials and Methods AnimalsH...

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MicroRNA-200a/200b Modulate High Glucose-Induced Endothelial Inflammation by Targeting O-linked N-Acetylglucosamine Transferase Expression

Cited by 42 publications

References 43 publications

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

MiR-200b attenuates IL-6 production through IKKβ and ZEB1 in human gingival fibroblasts

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

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