Evidence map›Paper›PMID 25325755›Full record

ArticleJournal of lipid research2014

Arachidonic acid-dependent gene regulation during preadipocyte differentiation controls adipocyte potential.

Evanthia Nikolopoulou, Georgia Papacleovoulou, Frederic Jean-Alphonse, Giulia Grimaldi, Malcolm G Parker, Aylin C Hanyaloglu, Mark Christian

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
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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

7 authors at 3 institutions in 1 country.

Evanthia NikolopoulouInstitute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK.
Georgia PapacleovoulouDivision of Women's Health, King's College London, London, UK.
Frederic Jean-AlphonseInstitute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK.
Giulia GrimaldiInstitute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK.
Malcolm G ParkerInstitute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK.
Aylin C HanyalogluInstitute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK.
Mark ChristianDivision of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry, UK.
Imperial College London · GBKing's College London · GBUniversity of Warwick · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H020233/1
6 · The paper itself

Abstract

Arachidonic acid (AA) is a major PUFA that has been implicated in the regulation of adipogenesis. We examined the effect of a short exposure to AA at different stages of 3T3-L1 adipocyte differentiation. AA caused the upregulation of fatty acid binding protein 4 (FABP4/aP2) following 24 h of differentiation. This was mediated by the prostaglandin F(2α) (PGF(2α)), as inhibition of cyclooxygenases or PGF(2α) receptor signaling counteracted the AA-mediated aP2 induction. In addition, calcium, protein kinase C, and ERK are all key elements of the pathway through which AA induces the expression of aP2. We also show that treatment with AA during the first 24 h of differentiation upregulates the expression of the transcription factor Fos-related antigen 1 (Fra-1) via the same pathway. Finally, treatment with AA for 24 h at the beginning of the adipocyte differentiation is sufficient to inhibit the late stages of adipogenesis through a Fra-1-dependent pathway, as Fra-1 knockdown rescued adipogenesis. Our data show that AA is able to program the differentiation potential of preadipocytes by regulating gene expression at the early stages of adipogenesis.

Indexed as

AdipogenesisGene Expression Regulation, Developmental3T3-L1 CellsAdipocytes, WhiteAnimalsArachidonic AcidCalcium SignalingDinoprostDown-RegulationFatty Acid-Binding ProteinsFos-Related Antigen 1KineticsMAP Kinase Signaling SystemMiceProtein Kinase CProto-Oncogene Proteins c-fosArachidonic AcidDinoprostFabp4 protein, mouseFatty Acid-Binding ProteinsFos-Related Antigen 1prostaglandin F2alpha receptorProtein Kinase CProto-Oncogene Proteins c-fosReceptors, ProstaglandinRNA, Small Interferingadipogenesiscell signalingmetabolismprostaglandins

Identifiers

PMID25325755
PMCPMC4242441
OpenAlexW2137062460

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.