Evidence map›Paper›PMID 22479536›Full record

ArticlePloS one2012

Activation of protein kinase A and exchange protein directly activated by cAMP promotes adipocyte differentiation of human mesenchymal stem cells.

Bingbing Jia, Lise Madsen, Rasmus Koefoed Petersen, Nathalie Techer, Reidun Kopperud, Tao Ma, Stein Ove Døskeland, Gérard Ailhaud, Jinfu Wang, Ez-Zoubir Amri and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Engineering Human Beige Adipose Tissue.Frontiers in bioengineering and biotechnology · 2022
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  4. Review
  5. Article
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  12. Protein kinase A induces UCP1 expression in specific adipose depots to increase energy expenditure and improve metabolic health.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Article
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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

11 authors at 5 institutions in 4 countries.

Bingbing JiaInstitute of Cell Biology and Genetics, College of Life Sciences, Zhejiang University, Hangzhou, People's Republic of China.
Lise Madsen
Rasmus Koefoed Petersen
Nathalie Techer
Reidun Kopperud
Tao Ma
Stein Ove Døskeland
Gérard Ailhaud
Jinfu Wang
Ez-Zoubir Amri
Karsten Kristiansen
University of Copenhagen · DKInserm · FRUniversity of Bergen · NOUniversité Côte d'Azur · FRZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human mesenchymal stem cells are primary multipotent cells capable of differentiating into several cell types including adipocytes when cultured under defined in vitro conditions. In the present study we investigated the role of cAMP signaling and its downstream effectors, protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac) in adipocyte conversion of human mesenchymal stem cells derived from adipose tissue (hMADS). We show that cAMP signaling involving the simultaneous activation of both PKA- and Epac-dependent signaling is critical for this process even in the presence of the strong adipogenic inducers insulin, dexamethasone, and rosiglitazone, thereby clearly distinguishing the hMADS cells from murine preadipocytes cell lines, where rosiglitazone together with dexamethasone and insulin strongly promotes adipocyte differentiation. We further show that prostaglandin I(2) (PGI(2)) may fully substitute for the cAMP-elevating agent isobutylmethylxanthine (IBMX). Moreover, selective activation of Epac-dependent signaling promoted adipocyte differentiation when the Rho-associated kinase (ROCK) was inhibited. Unlike the case for murine preadipocytes cell lines, long-chain fatty acids, like arachidonic acid, did not promote adipocyte differentiation of hMADS cells in the absence of a PPARγ agonist. However, prolonged treatment with the synthetic PPARδ agonist L165041 promoted adipocyte differentiation of hMADS cells in the presence of IBMX. Taken together our results emphasize the need for cAMP signaling in concert with treatment with a PPARγ or PPARδ agonist to secure efficient adipocyte differentiation of human hMADS mesenchymal stem cells.

Indexed as

Gene Expression Regulation1-Methyl-3-isobutylxanthineAdipocytesAdipose TissueAnimalsCell DifferentiationCell LineCyclic AMPCyclic AMP-Dependent Protein KinasesDexamethasoneEpoprostenolGene Expression ProfilingGuanine Nucleotide Exchange FactorsHumansInsulinMesenchymal Stem Cells1-Methyl-3-isobutylxanthineCyclic AMPCyclic AMP-Dependent Protein KinasesDexamethasoneEpoprostenolGuanine Nucleotide Exchange FactorsInsulinRAPGEF3 protein, humanRosiglitazoneThiazolidinediones

Identifiers

PMID22479536
PMCPMC3313974
OpenAlexW2064322206

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.