Evidence map›Paper›PMID 30710574›Full record

ArticleMetabolism: clinical and experimental2019

Inflammation and ER stress differentially regulate STAMP2 expression and localization in adipocytes.

Jørgen Sikkeland, Torstein Lindstad, Hatice Zeynep Nenseth, Xavier Dezitter, Su Qu, Ridhwan M Muhumed, Meric Erikci Ertunc, Margaret F Gregor, Fahri Saatcioglu

Abstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

9 authors.

Jørgen SikkelandDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway; Institute for Cancer Genetics and Informatics, Oslo University Hospital, 0310 Oslo, Norway.
Torstein LindstadDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway.
Hatice Zeynep NensethDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway.
Xavier DezitterPlateforme de Binding et de Biologie Moléculaire, Institut de Chimie Pharmaceutique Albert Lespagnol, Faculté des Sciences Pharmaceutiques et Biologiques - Université de Lille, F-59006 Lille, France.
Su QuDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway.
Ridhwan M MuhumedDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway.
Meric Erikci ErtuncDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway; Department of Genetics and Complex Diseases and Sabri Ülker Center, Harvard TH Chan School of Public Health, Boston, MA 02115, USA.
Margaret F GregorDepartment of Genetics and Complex Diseases and Sabri Ülker Center, Harvard TH Chan School of Public Health, Boston, MA 02115, USA.
Fahri SaatciogluDepartment of Biosciences, University of Oslo, Postboks 1066 Blindern, 0316 Oslo, Norway; Institute for Cancer Genetics and Informatics, Oslo University Hospital, 0310 Oslo, Norway. Electronic address: fahris@ibv.uio.no.

Funding

Interdisciplinary Training in Genetics & Complex DiseaseR90DK071507 · NIDDK · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI WESSLING-RESNICK, MARIANNE · 2004 to 2008
$1.1M
NIDDK NIH HHS R90 DK071507
6 · The paper itself

Abstract

backgroundChronic ER stress and dysfunction is a hallmark of obesity and a critical contributor to metaflammation, abnormal hormone action and altered substrate metabolism in metabolic tissues, such as liver and adipocytes. Lack of STAMP2 in lean mice induces inflammation and insulin resistance on a regular diet, and it is dysregulated in the adipose tissue of obese mice and humans. We hypothesized that the regulation of STAMP2 is disrupted by ER stress.

methods3T3-L1 and MEF adipocytes were treated with ER stress inducers thapsigargin and tunicamycin, and inflammation inducer TNFα. The treatments effect on STAMP2 expression and enzymatic function was assessed. In addition, 3T3-L1 adipocytes and HEK cells were utilized for Stamp2 promoter activity investigation performed with luciferase and ChIP assays.

resultsER stress significantly reduced both STAMP2 mRNA and protein expression in cultured adipocytes whereas TNFα had the opposite effect. Concomitant with loss of STAMP2 expression during ER stress, intracellular localization of STAMP2 was altered and total iron reductase activity was reduced. Stamp2 promoter analysis by reporter assays and chromatin immunoprecipitation, showed that induction of ER stress disrupts C/EBPα-mediated STAMP2 expression.

conclusionThese data suggest a clear link between ER stress and quantitative and functional STAMP2-deficiency.

Indexed as

Endoplasmic Reticulum StressAdipocytesAnimalsCells, CulturedInflammationMembrane ProteinsMiceRNA, MessengerThapsigarginTumor Necrosis Factor-alphaMembrane ProteinsRNA, MessengerThapsigarginTiarp protein, mouseTumor Necrosis Factor-alphaAdipocyteER stressGene expressionIron reductaseProtein translocationSTAMP2

Identifiers

PMID30710574
PMCPMC6460919

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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.