Evidence map›Paper›PMID 8601591›Full record

ArticleThe Journal of cell biology1996

Differentially expressed fibroblast growth factors regulate skeletal muscle development through autocrine and paracrine mechanisms.

K Hannon, A J Kudla, M J McAvoy, K L Clase, B B Olwin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-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

50 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. MyoD Over-Expression Rescues GST-bFGF Repressed Myogenesis.International journal of molecular sciences · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. The emergence of the stem cell niche.Trends in cell biology · 2023
    Review
  9. Article
  10. Article
  11. FGF-2-dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Review
  13. Article
  14. Review
  15. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  16. Article
  17. Fibrocyte accumulation in the lungs of cystic fibrosis patients.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Article
  18. Review
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

K HannonDepartment of Biochemistry, Purdue University, West Lafayette, Indiana 47907, USA.
A J Kudla
M J McAvoy
K L Clase
B B Olwin
Purdue University West Lafayette · US

Funding

MYOGENIC GRWOTH AND DIFFERENTIATIONR01AR039467 · NIAMS · UNIVERSITY OF COLORADO AT BOULDER · PI OLWIN, BRADLEY B · 1994 to 2008
$2.8M
ANALYSIS OF MYOGENIC GROWTH AND DIFFERENTIATIONR29AR039467 · NIAMS · UNIVERSITY OF WISCONSIN MADISON · PI OLWIN, BRADLEY B · 1988 to 1992
–
NIAMS NIH HHS AR39467
6 · The paper itself

Abstract

Several FGF family members are expressed in skeletal muscle; however, the roles of these factors in skeletal muscle development are unclear. We examined the RNA expression, protein levels, and biological activities of the FGF family in the MM14 mouse skeletal muscle cell line. Proliferating skeletal muscle cells express FGF-1, FGF-2, FGF-6, and FGF-7 mRNA. Differentiated myofibers express FGF-5, FGF-7, and reduced levels of FGF-6 mRNA. FGF-3, FGF-4, and FGF-8 were not detectable by RT-PCR in either proliferating or differentiated skeletal muscle cells. FGF-I and FGF-2 proteins were present in proliferating skeletal muscle cells, but undetectable after terminal differentiation. We show that transfection of expression constructs encoding FGF-1 or FGF-2 mimics the effects of exogenously applied FGFs, inhibiting skeletal muscle cell differentiation and stimulating DNA synthesis. These effects require activation of an FGF tyrosine kinase receptor as they are blocked by transfection of a dominant negative mutant FGF receptor. Transient transfection of cells with FGF-1 or FGF-2 expression constructs exerted a global effect on myoblast DNA synthesis, as greater than 50% of the nontransfected cells responded by initiating DNA synthesis. The global effect of cultures transfected with FGF-2 expression vectors was blocked by an anti-FGF-2 monoclonal antibody, suggesting that FGF-2 was exported from the transfected cells. Despite the fact that both FGF-l and FGF-2 lack secretory signal sequences, when expressed intracellularly, they regulate skeletal muscle development. Thus, production of FGF-1 and FGF-2 by skeletal muscle cells may act as a paracrine and autocrine regulator of skeletal muscle development in vivo.

Indexed as

ActinsAnimalsBase SequenceCell DifferentiationCell DivisionCell LineFibroblast Growth FactorsGenes, ReporterMiceMolecular Sequence DataMuscle ProteinsMuscle, SkeletalPromoter Regions, GeneticReceptors, Fibroblast Growth FactorRecombinant Fusion ProteinsSignal TransductionActinsFibroblast Growth FactorsMuscle ProteinsReceptors, Fibroblast Growth FactorRecombinant Fusion Proteins

Identifiers

PMID8601591
PMCPMC2120753
OpenAlexW2078164924

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.