Evidence map›Paper›PMID 18591389›Full record

ArticleDiabetes2008

Neuronatin: a new inflammation gene expressed on the aortic endothelium of diabetic mice.

Nino Mzhavia, Shuiqing Yu, Shota Ikeda, Tehua T Chu, Ira Goldberg, Hayes M Dansky

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

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  13. Characteristic Localization of Neuronatin in Rat Testis, Hair Follicle, Tongue, and Pancreas.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Article
  14. PPARMediators of inflammation · 2019
    Article
  15. Article
  16. High neuronatin (NNAT) expression is associated with poor outcome in breast cancer.Virchows Archiv : an international journal of pathology · 2017
    Article
  17. Article
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Nino MzhaviaDivision of Cardiology, Columbia University, New York, New York, USA. nm2170@columbia.edu
Shuiqing Yu
Shota Ikeda
Tehua T Chu
Ira Goldberg
Hayes M Dansky
Columbia University · USIcahn School of Medicine at Mount Sinai · US

Funding

Role of leptin in atherosclerosis and arterial injuryR01HL073191 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GOLDBERG, IRA · 2003 to 2007
$2.0M
NHLBI NIH HHS HL073191NHLBI NIH HHS R01 HL073191
6 · The paper itself

Abstract

objectiveIdentification of arterial genes and pathways altered in obesity and diabetes. RESEARCH DESIGN AND

methodsAortic gene expression profiles of obese and diabetic db/db, high-fat diet-fed C57BL/6J, and control mice were obtained using mouse Affymetrix arrays. Neuronatin (Nnat) was selected for further analysis. To determine the function of Nnat, a recombinant adenovirus (Ad-Nnat) was used to overexpress the Nnat gene in primary endothelial cells and in the mouse aorta in vivo.

resultsNnat, a gene of unknown vascular function, was upregulated in the aortas of db/db and high-fat diet-fed mice. Nnat gene expression was increased in db/db mouse aorta endothelial cells. Nnat protein was localized to aortic endothelium and was selectively increased in the endothelium of db/db mice. Infection of primary human aortic endothelial cells (HAECs) with Ad-Nnat increased expression of a panel of nuclear factor-kappaB (NF-kappaB)-regulated genes, including inflammatory cytokines, chemokines, and cell adhesion molecules. Infection of mouse carotid arteries in vivo with the Ad-Nnat increased expression of vascular cell adhesion molecule 1 protein. Nnat activation of NF-kappaB and inflammatory gene expression in HAECs was mediated through pathways distinct from tumor necrosis factor-alpha. Nnat expression stimulated p38, Jun NH(2)-terminal kinase, extracellular signal-related kinase, and AKT kinase phosphorylation. Phosphatidylinositol 3-kinase and p38 inhibitors prevented Nnat-mediated activation of NF-kappaB-induced gene expression.

conclusionsNnat expression is increased in endothelial cells of obese and diabetic mouse blood vessels. The effects of Nnat on inflammatory pathways in vitro and in vivo suggest a pathophysiological role of this new gene in diabetic vascular diseases.

Indexed as

AdenoviridaeAnimalsAortaBlotting, WesternCells, CulturedChemokinesCytokinesDiabetes MellitusDietary FatsDisease Models, AnimalEndothelial CellsGene ExpressionGene Expression ProfilingGenetic VectorsImmunohistochemistryInflammation MediatorsChemokinesCytokinesDietary FatsInflammation MediatorsMembrane ProteinsNerve Tissue ProteinsNnat protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID18591389
PMCPMC2551689
OpenAlexW2124203337

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.