Evidence map›Paper›PMID 25156632›Full record

ArticleBMC neuroscience2014

Growth hormone pathways signaling for cell proliferation and survival in hippocampal neural precursors from postnatal mice.

Pablo Devesa, Fabienne Agasse, Sara Xapelli, Cristina Almengló, Jesús Devesa, Joao O Malva, Víctor M Arce

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  16. Growth Hormone (GH) and Cardiovascular System.International journal of molecular sciences · 2018
    Review
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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

7 authors at 3 institutions in 3 countries.

Pablo Devesa
Fabienne Agasse
Sara Xapelli
Cristina Almengló
Jesús DevesaDepartment of Physiology, School of Medicine, University of Santiago de Compostela, 15710 Santiago de Compostela, Spain. jesus.devesa@usc.es.
Joao O Malva
Víctor M Arce
Universidade de Santiago de Compostela · ESUniversity of Coimbra · PTTetra Tech (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence suggests that growth hormone (GH) may play a major role in the regulation of postnatal neurogenesis, thus supporting the possibility that it may be also involved in promoting brain repair after brain injury. In order to gain further insight on this possibility, in this study we have investigated the pathways signaling the effect of GH treatment on the proliferation and survival of hippocampal subgranular zone (SGZ)-derived neurospheres.

resultsOur results demonstrate that GH treatment promotes both proliferation and survival of SGZ neurospheres. By using specific chemical inhibitors we have been also able to demonstrate that GH treatment promotes the activation of both Akt-mTOR and JNK signaling pathways, while blockade of these pathways either reduces or abolishes the GH effects. In contrast, no effect of GH on the activation of the Ras-ERK pathway was observed after GH treatment, despite blockade of this signaling path also resulted in a significant reduction of GH effects. Interestingly, SGZ cells were also capable of producing GH, and blockade of endogenous GH also resulted in a decrease in the proliferation and survival of SGZ neurospheres.

conclusionsAltogether, our findings suggest that GH treatment may promote the proliferation and survival of neural progenitors. This effect may be elicited by cooperating with locally-produced GH in order to increase the response of neural progenitors to adequate stimuli. On this view, the possibility of using GH treatment to promote neurogenesis and cell survival in some acquired neural injuries may be envisaged.

Indexed as

AnimalsApoptosisCell ProliferationCells, CulturedCell SurvivalExtracellular Signal-Regulated MAP KinasesGrowth HormoneHippocampusHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMice, Inbred C57BLNeural Stem CellsNeurogenesisPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsExtracellular Signal-Regulated MAP KinasesGrowth HormoneJNK Mitogen-Activated Protein KinasesmTOR protein, mousePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktras ProteinsRecombinant ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID25156632
PMCPMC4155078
OpenAlexW2136248784

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.