Involvement of miR-539-5p in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue

Gràcia, Ana; Miranda, Jonatan; Fernández‐Quintela, Alfredo; Eseberri, Itziar; Garcia-Lacarte, Marcos; Milagro, Fermı́n I.; Martínéz, J. Alfredo; Aguirre, Leixuri; Portillo, Marı́a P.

doi:10.1039/c5fo01090j

Cited by 41 publications

(26 citation statements)

References 53 publications

(50 reference statements)

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“…Consistent with the critical role of CXCR7 in angiogenesis, we found that, by targeting CXCR7 pathways, miR-539-5p represses angiogenesis both in vitro and in vivo; therefore, we provide new evidence for understanding miR-539-5p as it functions as an angiogenic suppressor. Of interest, a recent study indicated that miR-539-5p is involved in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue (52). Resveratrol has been confirmed to suppress CNV development in several animal studies (53,54), and, therefore, we speculated that the changes in miR-539-5p levels may be a possible mechanism for the inhibitory effect of resveratrol.…”

Section: Discussionmentioning

confidence: 86%

miR‐539‐5p inhibits experimental choroidal neovascularization by targeting CXCR7

et al. 2018

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Stromal cell-derived factor-1 (SDF-1) has been previously confirmed to participate in the formation of choroidal neovascularization (CNV) via its receptor, CXC chemokine receptor (CXCR) 4; CXCR7 is a recently identified receptor for SDF-1. The molecular mechanisms and therapeutic value of CXCR7 in CNV remain undefined. In this study, experimental CNV was induced by laser photocoagulation in Brown-Norway pigmented rats, and aberrant CXCR7 overexpression was detected in the retinal pigment epithelial/choroid/sclera tissues of laser-injured eyes. Blockade of CXCR7 activation via CXCR7 knockdown or neutralizing Ab administration inhibited SDF-1-induced cell survival and the tubular formation of human retinal microvascular endothelial cells (HRMECs) in vitro and reduced CNV leakage and lesion size in vivo. By using microRNA array screening and bioinformatic analyses, we identified miR-539-5p as a regulator of CXCR7. Transfection of HRMECs and choroid-retinal endothelial (RF/6A) cells with the miR-539-5p mimic inhibited their survival and tube formation, whereas CXCR7 overexpression rescued the suppressive effect of miR-539-5p. The antiangiogenic activities of the miR-539-5p mimic were additionally demonstrated in vivo by intravitreal injection. ERK1/2 and AKT signaling downstream of CXCR7 is involved in the miR-539-5p regulation of endothelial cell behaviors. These findings suggest that the manipulation of miR-539-5p/CXCR7 levels may have important therapeutic implications in CNV-associated diseases.-Feng, Y., Wang, J., Yuan, Y., Zhang, X., Shen, M., Yuan, F. miR-539-5p inhibits experimental choroidal neovascularization by targeting CXCR7.

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Section: Discussionmentioning

confidence: 86%

miR‐539‐5p inhibits experimental choroidal neovascularization by targeting CXCR7

et al. 2018

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“…miRNA kit (R7034-02; Omega Bio-Tek, Norcross, GA, USA) according to the manufacturer’s instructions. Total RNA (9 ng) was reverse-transcribed using the TaqMan MicroRNA Reverse Transcription kit (Applied Biosystems, Foster City, CA, USA), as previously reported in Gracia et al [27]. The targeted miRNA assay sequences were as follows (source miRBase):

rno-miRNA-103-3p: 5′-AGCAGCAUUGUACAGGGCUAUGA-3′

rno-miRNA-107-3p: 5′-AGCAGCAUUGUACAGGGCUAUCA-3′

rno-miRNA-122-5p: 5′-UGGAGUGUGACAAUGGUGUUUG-3′

…”

Section: Methodsmentioning

confidence: 99%

“…In the case of AML12 cells, total protein was extracted with 200 µL of lysis buffer as previously reported [27]. Protein concentration was measured by BCA protein assay kit (Thermo Scientific, Wilmington, DE, USA).…”

Section: Methodsmentioning

confidence: 99%

Are miRNA-103, miRNA-107 and miRNA-122 Involved in the Prevention of Liver Steatosis Induced by Resveratrol?

et al. 2017

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The aim of the present study was to determine whether the reduction in liver fat previously observed in our laboratory in a cohort of rats which had been fed an obesogenic diet was mediated by changes in the expression of microRNA (miRNA)-103-3p, miRNA-107-3p and miRNA-122-5p, which represent 70% of total miRNAs in the liver, as well as in their target genes. The expression of the three analysed miRNAs was reduced in rats treated with resveratrol. A reduction in sterol-regulatory element binding protein 1 (SREBP1) and an increase in carnitine palmitoyltransferase 1a (CPT1a) were observed in resveratrol-treated rats. No changes were found in fatty acid synthase (FAS). In cultured hepatocytes, SREBP1 protein was increased after the transfection of each miRNA. FAS protein expression was decreased after the transfection of miRNA-122-5p, and CPT1a protein was down-regulated by the over-expression of miRNA-107-3p. This study provides new evidences which show that srebf1 is a target gene for miRNA-103-3p and miRNA-107-3p, fasn a target gene for miRNA-122-5p and cpt1a a target gene for miRNA-107-3p. Moreover, the reduction in liver steatosis induced by resveratrol in rats fed an obesegenic diet is mediated, at least in part, by the increase in CPT1a protein expression and activity, via a decrease in miRNA-107-3p expression.

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“…The microarray showed that 3 miRNAs were decreased and 13 were increased after resveratrol treatment. Among those miRNAs increased, miR‐129, miR‐328‐5p, and miR‐539‐5p showed predicted target genes (pparγ: peroxisome proliferator‐activated receptor gamma, hsl: hormone sensitive lipase and sp1: SP1 transcription factor) relevant for triacylglycerol metabolism in WAT in the miRWalk database .…”

Section: Micrornasmentioning

confidence: 99%

Chemoprevention by resveratrol and pterostilbene: Targeting on epigenetic regulation

Lee

Chiou

et al. 2017

BioFactors

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Epigenetic mechanisms are essential in regulating normal cellular functions and play an important role during the disease developmental stages. However, aberrant epigenetic mechanisms may lead to pathological consequences such as cancer, neurological disorders, bone and skeletal diseases, cardiovascular dysfunction, and metabolic syndrome. The molecular mechanisms of epigenetic modification include DNA methylation, histone modification (acetylation, methylation and phosphorylation), and microRNAs (miRNAs). Unlike genetic modifications, epigenetic states of genes are reversible and can be altered by certain intrinsic and extrinsic factors. In the past few decades, accumulated evidence shows that dietary phytochemicals with chemopreventive effects are also potent epigenetic regulators. Resveratrol and pterostilbene are stilbenoids, which have been reported to have anti-cancer, antiinflammatory, anti-lipid, and anti-diabetic properties. Stilbenoids are also reported to improve cardiovascular disease. By altering DNA methylation and histone modification or by modulating miRNA expression, resveratrol, and pterostilbene become potent epigenetic modifiers. In this review, we summarize these studies and underlying mechanisms of resveratrol and pterostilbene and their influence on epigenetic mechanisms. V C 2017 BioFactors, 44(1): [26][27][28][29][30][31][32][33][34][35] 2018 Keywords: epigenetic; chemoprevention; resveratrol; pterostilbene Abbreviations: 3 0 UTR, 3 0 untranslated region; Ago2, argonaute2; AhR, aromatic hydrocarbon receptor; AMPK, AMP activated protein kinase; AP-1, activator protein-1; ARH-I, aplasia Ras homolog member I; AURKA, aurora kinase; BCL-2, B-cell lymphoma 2; BMFs, buccal mucosal fibroblasts; BRCA-1, breast cancer type 1; CAD, coronary artery disease; CCNB1, cyclin B1; CDKs, cyclin-dependent kinase; CLU, clusterin; CRP, C-reactive protein; CSCs, cancer stem cells; DMNTs, DNA methyltransferases; eNOS, endothelial NOS; ERa, estrogen receptor-alpha; EZH2, enhancer of zeste homolog 2; GBM, glioblastoma multiforme; GSCs, glioma stem cells; H3K9, acetyl-H3lysine9; HAT, histone acetyl transferase; HDACs, type III histone deacetylases; HK2, hexokinase 2; HSL, hormone sensitive lipase; MCP-1, monocyte hemoattractant protein-1; miRNAs, MicroRNAs; MNNG, N-methyl-N 0 -nitro-N-nitrosoguanidine; MTA1, metastasis-associated protein 1; NAD 1 , nicotinamide adenine dinucleotide 1 ; NAFLD, nonalcoholic fatty liver disease; NGFR, nerve growth factor receptor; NO, nitric oxide; NuRD, nucleosome remodeling deacetylation; OSF, oral submucous fibrosis; PDCD4, programmed cell death protein 4; PGR, progesterone receptor gene; PPARc, peroxisome proliferator-activated receptor gamma; PTEN, phosphatase and tensin homolog; RANKL, receptor activator of NF-jB ligand; RASSF1A, Ras association domain-containing protein 1; RNAi, RNA interference; SAM, S-adenosyl-l-methionine; SERCA2a, sarcoplasmic/endoplasmic reticulum Ca(21)ATPase 2a; sirtuins, silent information regulator 2-related proteins; SMADs, SMA and Mad rel...

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Involvement of miR-539-5p in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue

Cited by 41 publications

References 53 publications

miR‐539‐5p inhibits experimental choroidal neovascularization by targeting CXCR7

miR‐539‐5p inhibits experimental choroidal neovascularization by targeting CXCR7

Are miRNA-103, miRNA-107 and miRNA-122 Involved in the Prevention of Liver Steatosis Induced by Resveratrol?

Chemoprevention by resveratrol and pterostilbene: Targeting on epigenetic regulation

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