Evidence map›Paper›PMID 25857555›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

TNF-related apoptosis-inducing ligand promotes human preadipocyte proliferation via ERK1/2 activation.

Jan-Bernd Funcke, Verena Zoller, Muad Abd El Hay, Klaus-Michael Debatin, Martin Wabitsch, Pamela Fischer-Posovszky

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Obesity and Bone Health: A Complex Relationship.International journal of molecular sciences · 2022
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Impacts of Alternative Splicing Events on the Differentiation of Adipocytes.International journal of molecular sciences · 2015
    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.

Jan-Bernd Funcke*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany.
Verena Zoller*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany.
Muad Abd El Hay*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany.
Klaus-Michael Debatin*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany.
Martin Wabitsch*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany.
Pamela Fischer-Posovszky*Division of Pediatric Endocrinology and Diabetes and Department of Pediatrics and Adolescent Medicine, Ulm Medical Center, Ulm, Germany pamela.fischer@uniklinik-ulm.de.
University Hospital Ulm · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon obesity, adipose tissue is excessively expanded and characterized by pathologic processes like hypoxia, fibrosis, and inflammation. Death ligands belonging to the TNF superfamily such as TNF-α are important contributors to these derangements and exert a pronounced influence on the metabolic and cellular homeostasis of adipose tissue. Here, we sought to identify the effect of the death ligand TNF-related apoptosis-inducing ligand (TRAIL) on the adipose tissue precursor cell pool and therefore investigated its influence on preadipocyte proliferation. Treatment of human preadipocytes with TRAIL resulted in a time- and dose-dependent increase in proliferation (EC50 3.4 ng/ml) comparable to IGF-1. Although no apoptosis was observed, TRAIL triggered a rapid cleavage of caspase-8 and -3. Neither inhibition of caspase activity by zVAD.fmk (20 µM) nor ablation of caspase-8 expression by lentivirus-delivered small hairpin RNA (shRNA) abolished the proliferative response. TRAIL triggered a delayed and sustained activation of ERK1/2, leaving Akt, p38, JNK, and NF-κB unaffected. Importantly, inhibition of ERK1/2 activation by PD0325901 (300 nM) or AZD6244 (5 or 10 µM) completely abolished the proliferative response. We thus reveal a hitherto unknown function of TRAIL in regulating adipose tissue homeostasis by promoting the proliferation of tissue-resident precursor cells.

Indexed as

MAP Kinase Signaling SystemAdipocytes, WhiteAdultAdult Stem CellsArrhythmias, CardiacBenzamidesBenzimidazolesCaspase 8Cell ProliferationCells, CulturedDiphenylamineFemaleGenetic Diseases, X-LinkedGigantismHeart Defects, CongenitalHumansAZD 6244BenzamidesBenzimidazolesCASP8 protein, humanCaspase 8DiphenylaminemirdametinibNF-kappa BProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRNARNA, recombinantTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanadipocyte progenitoradipose tissue homeostasisdeath ligandnoncanonical signaling

Identifiers

PMID25857555
PMCPMC4478800
OpenAlexW1983914631

What OpenQuestion holds

Textmetadata
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.