Evidence map›Paper›PMID 30347224›Full record

ArticleCellular signalling2019

Dual-specificity phosphatases regulate mitogen-activated protein kinase signaling in adipocytes in response to inflammatory stress.

Bradley S Ferguson, Heesun Nam, Ron F Morrison

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Protective effect of α-asarone and β-asarone on Aβ -induced inflammatory response in PC12 cells and its.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Bradley S FergusonDepartment of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402, United States.
Heesun NamDepartment of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402, United States.
Ron F MorrisonDepartment of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402, United States. Electronic address: rfmorris@uncg.edu.
University of North Carolina at Greensboro · US

Funding

Regulation of JNK Signaling by Dual Specificity Phosphatases in AdipocytesR15DK082799 · NIDDK · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI MORRISON, RON F · 2010 to 2010
$209k
Role of DUSPs in adipocytes in response to inflammatory stress.F31DK084770 · NIDDK · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI FERGUSON, BRADLEY S · 2009 to 2010
$56k
NIDDK NIH HHS F31 DK084770NIDDK NIH HHS R15 DK082799
6 · The paper itself

Abstract

Obesity is a strong predictor of heart disease, insulin resistance, and type II diabetes. Chronic, low-grade inflammation links obesity and insulin resistance through mitogen-activated protein kinase (MAPK) signaling pathways. Upstream kinases activate MAPK signaling, while MAPK-specific dual-specificity phosphatases (DUSPs) act as key modulators and controllers of MAPK deactivation (i.e. dephosphorylation). Using tumor necrosis factor α (TNFα) in 3 T3-L1 adipocytes as a model of inflammation, we report that TNFα-mediated induction of Dusp1, Dusp8 and Dusp16 modulated the transient regulation of MAPK (i.e., ERK, JNK, and p38) phosphorylation and subsequent inflammatory gene expression. All three MAPKs examined were phosphorylated in preadipocytes and adipocytes in response to TNFα, where signaling magnitude and duration were phenotype-specific. Moreover, TNFα increased mRNA abundance of DUSPs in preadipocytes and adipocytes in a phenotype-specific manner, concomitant with dephosphorylation of MAPKs. RNA interference (RNAi)-mediated knockdown of Dusp1, Dusp8 and Dusp16 increased signaling magnitude and duration of ERK, JNK, and p38 that subsequently resulted in significant increases in MAPK-dependent inflammatory gene expression of MCP-1, IL-6, and Cox-2 in response to TNFα. This study highlights important roles for DUSPs as integral components of MAPK signaling and adipocyte inflammatory gene expression.

Indexed as

MAP Kinase Signaling System3T3-L1 CellsAdipocytesAnimalsDual-Specificity PhosphatasesInflammationMiceMitogen-Activated Protein KinasesPhosphorylationTumor Necrosis Factor-alphaDual-Specificity PhosphatasesMitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID30347224
PMCPMC9590594
OpenAlexW2897668352

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.