Evidence map›Paper›PMID 26878848›Full record

ArticleNeural development2016

Region-specific role of growth differentiation factor-5 in the establishment of sympathetic innervation.

Gerard W O'Keeffe, Humberto Gutierrez, Laura Howard, Christopher W Laurie, Catarina Osorio, Núria Gavaldà, Sean L Wyatt, Alun M Davies

Open access · goldAbstract read
In one paragraph

Article in Neural development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022
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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

8 authors at 2 institutions in 3 countries.

Gerard W O'KeeffeSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Humberto GutierrezSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Laura HowardSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Christopher W LaurieSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Catarina OsorioSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Núria GavaldàSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Sean L WyattSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK.
Alun M DaviesSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT, UK. daviesalun@cf.ac.uk.
Cardiff University · GBSOM Biotech (Spain) · ES

Funding

Wellcome Trust 103852
6 · The paper itself

Abstract

backgroundNerve growth factor (NGF) is the prototypical target-derived neurotrophic factor required for sympathetic neuron survival and for the growth and ramification of sympathetic axons within most but not all sympathetic targets. This implies the operation of additional target-derived factors for regulating terminal sympathetic axon growth and branching.

resultsHere report that growth differentiation factor 5 (GDF5), a widely expressed member of the transforming growth factor beta (TGFβ) superfamily required for limb development, promoted axon growth from mouse superior cervical ganglion (SCG) neurons independently of NGF and enhanced axon growth in combination with NGF. GDF5 had no effect on neuronal survival and influenced axon growth during a narrow window of postnatal development when sympathetic axons are ramifying extensively in their targets in vivo. SCG neurons expressed all receptors capable of participating in GDF5 signaling at this stage of development. Using compartment cultures, we demonstrated that GDF5 exerted its growth promoting effect by acting directly on axons and by initiating retrograde canonical Smad signalling to the nucleus. GDF5 is synthesized in sympathetic targets, and examination of several anatomically circumscribed tissues in Gdf5 null mice revealed regional deficits in sympathetic innervation. There was a marked, highly significant reduction in the sympathetic innervation density of the iris, a smaller though significant reduction in the trachea, but no reduction in the submandibular salivary gland. There was no reduction in the number of neurons in the SCG.

conclusionsThese findings show that GDF5 is a novel target-derived factor that promotes sympathetic axon growth and branching and makes a distinctive regional contribution to the establishment of sympathetic innervation, but unlike NGF, plays no role in regulating sympathetic neuron survival.

Indexed as

Activin Receptors, Type IIAnimalsAxonsBone Morphogenetic Protein ReceptorsCells, CulturedFemaleGrowth Differentiation Factor 5IrisMaleMiceMice, Inbred C57BLMice, KnockoutSalivary GlandsSignal TransductionSmad ProteinsSuperior Cervical GanglionActivin Receptors, Type IIactivin receptor type II-ABone Morphogenetic Protein ReceptorsGdf5 protein, mouseGrowth Differentiation Factor 5Smad Proteins

Identifiers

PMID26878848
PMCPMC4755026
OpenAlexW2278917784

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.