Evidence map›Paper›PMID 22700586›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2012

BDNF alters ERK/p38 MAPK activity ratios to promote differentiation in growth plate chondrocytes.

Michele R Hutchison

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. p75Science advances · 2026
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  11. Novel Loss-of-Function Mutations inFrontiers in genetics · 2022
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  13. αFrontiers in cell and developmental biology · 2020
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  16. Molecular therapeutic strategies for FGFR3 gene-related skeletal dysplasia.Journal of molecular medicine (Berlin, Germany) · 2017
    Review
  17. Article
  18. Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    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

1 author at 1 institution in 1 country.

Michele R HutchisonDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA. michele.hutchison@utsouthwestern.edu
The University of Texas Southwestern Medical Center · US

Funding

Examination of the Pre-pubertal Mammalian Growth PlateK08DK073447 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HUTCHISON, MICHELE REBECCA · 2006 to 2010
$614k
NIDDK NIH HHS DK073447NIDDK NIH HHS K08 DK073447
6 · The paper itself

Abstract

The ERK and p38 MAPK pathways are well-known transducers of signals that regulate proliferation and differentiation, but precisely how these pathways control growth plate chondrocyte development is unclear. For example, the ERK pathway has been reported to be required by some investigators but inhibitory to chondrocyte development by others. Moreover, how these two pathways interact to regulate chondrocyte development is even less clear. Using primary bovine growth plate chondrocytes and murine ATDC5 cells, we demonstrate that the ERK and p38 pathways have opposing effects on proliferation but are both absolutely required for differentiation. Two factors that promote chondrocyte differentiation, brain-derived neurotrophic factor (BDNF) and C-type natriuretic peptide, increase p38 activity while decreasing, but not completely inhibiting, ERK activity. The attenuation of ERK activity by BDNF occurs via p38-dependent raf-1 inhibition. The inhibition of raf-1 by p38 is direct, because purified p38 protein inhibits the kinase activity of purified active raf-1 as well as raf-1 immunoprecipitated from chondrocyte lysates. Moreover, IGF-I, which stimulates proliferation, suppresses p38 activation. This work describes a model wherein unopposed IGF-I promotes high ERK/p38 activity ratios favoring proliferation, whereas BDNF signals a transition to differentiation by decreasing the ERK/p38 activity ratio without completely inhibiting ERK, which involves the direct inhibition of raf-1 by p38.

Indexed as

Cell DifferentiationAnimalsBrain-Derived Neurotrophic FactorCattleCells, CulturedChondrocytesEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGrowth PlateInsulinInsulin-Like Growth Factor IJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMiceNatriuretic Peptide, C-TypeBrain-Derived Neurotrophic FactorExtracellular Signal-Regulated MAP KinasesInsulinInsulin-Like Growth Factor IJNK Mitogen-Activated Protein KinasesNatriuretic Peptide, C-Typep38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-raf

Identifiers

PMID22700586
PMCPMC3404299
OpenAlexW1985901055

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.