Evidence map›Paper›PMID 25183006›Full record

ArticleThe Journal of biological chemistry2014

Natural antisense transcript for hyaluronan synthase 2 (HAS2-AS1) induces transcription of HAS2 via protein O-GlcNAcylation.

Davide Vigetti, Sara Deleonibus, Paola Moretto, Timothy Bowen, Jens W Fischer, Maria Grandoch, Alexander Oberhuber, Dona C Love, John A Hanover, Raffaella Cinquetti and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 129 citations in OpenAlex.

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  16. Role of long non-coding RNAs in adipogenesis: State of the art and implications in obesity and obesity-associated diseases.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2021
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  18. Role ofPhysiological reviews · 2021
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

Davide VigettiFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Sara DeleonibusFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Paola MorettoFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Timothy BowenDepartment of Nephrology, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, United Kingdom.
Jens W FischerInstitute of Pharmacology and Clinical Pharmacology, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany.
Maria GrandochInstitute of Pharmacology and Clinical Pharmacology, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany.
Alexander OberhuberDepartment of Vascular and Endovascular Surgery, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Dona C LoveLaboratory of Cell Biochemistry and Biology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
John A HanoverLaboratory of Cell Biochemistry and Biology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Raffaella CinquettiDipertimento di Biotecnologia e Scienze della Vita, Università degli Studi dell'Insubria, 21100 Varese, Italy, and.
Eugenia KarousouFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Manuela ViolaFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Maria Luisa D'AngeloFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Vincent C HascallBiomedical Engineering ND20, The Cleveland Clinic, Cleveland, Ohio 44195.
Giancarlo De LucaFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy.
Alberto PassiFrom the Dipartimento di Scienze Chirurgiche e Morfologiche, Università degli Studi dell'Insubria, Varese, Italy, alberto.passi@uninsubria.it.
University of Insubria · ITHeinrich Heine University Düsseldorf · DENational Institute of Diabetes and Digestive and Kidney Diseases · USCardiff University · GBCleveland Clinic · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Enzymes of O-GlcNAc cycling linked to type-2 diabetes and neurodegenerationZIADK060103 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$20.8M
VERSICAN PROTEOLYSIS AND REGULATION OF VASCULAR SMOOTH MUSCLEP01HL107147 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI LAUER, MARK E · 2011 to 2017
$16.1M
Calmodulin-driven Nuclear Trafficking linked to diabetes and insulin signalingZIADK060102 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$8.5M
NHLBI NIH HHS P01 HL107147
6 · The paper itself

Abstract

Changes in the microenvironment organization within vascular walls are critical events in the pathogenesis of vascular pathologies, including atherosclerosis and restenosis. Hyaluronan (HA) accumulation into artery walls supports vessel thickening and is involved in many cardiocirculatory diseases. Excessive cytosolic glucose can enter the hexosamine biosynthetic pathway, increase UDP-N-acetylglucosamine (UDP-GlcNAc) availability, and lead to modification of cytosolic proteins via O-linked attachment of the monosaccharide β-N-GlcNAc (O-GlcNAcylation) from UDP-GlcNAc by the enzyme O-GlcNAc transferase. As many cytoplasmic and nuclear proteins can be glycosylated by O-GlcNAc, we studied whether the expression of the HA synthases that synthesize HA could be controlled by O-GlcNAcylation in human aortic smooth muscle cells. Among the three HAS isoenzymes, only HAS2 mRNA increased after O-GlcNAcylation induced by glucosamine treatments or by inhibiting O-GlcNAc transferase with PUGNAC (O-(2-acetamido-2-deoxy-d-glucopyranosylidene)amino-N-phenylcarbamate). We found that the natural antisense transcript of HAS2 (HAS2-AS1) was absolutely necessary to induce the transcription of the HAS2 gene. Moreover, we found that O-GlcNAcylation modulated HAS2-AS1 promoter activation by recruiting the NF-κB subunit p65, but not the HAS2 promoter, whereas HAS2-AS1 natural antisense transcript, working in cis, regulated HAS2 transcription by altering the chromatin structure around the HAS2 proximal promoter via O-GlcNAcylation and acetylation. These results indicate that HAS2 transcription can be finely regulated not only by recruiting transcription factors to the promoter as previously described but also by modulating chromatin accessibility by epigenetic modifications.

Indexed as

Gene Expression Regulation, EnzymologicAcetylglucosamineAnimalsAortaBase SequenceCell NucleusChromatinCytoplasmEpigenesis, GeneticGene SilencingGlucuronosyltransferaseHumansHyaluronan SynthasesMaleMiceMice, KnockoutAcetylglucosamineChromatinGlucuronosyltransferaseHAS2 protein, humanHas2 protein, mouseHyaluronan SynthasesMonosaccharidesN-AcetylglucosaminyltransferasesO-GlcNAc transferaseRNA, MessengerEpigeneticsGlycobiologyGlycosaminoglycanGlycosylationHyaluronanLong Noncoding RNA (Long ncRNA, lncRNA)Proteoglycan

Identifiers

PMID25183006
PMCPMC4200242
OpenAlexW1965611576

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.