Evidence map›Paper›PMID 22292041›Full record

ArticlePloS one2012

AKT signaling mediates IGF-I survival actions on otic neural progenitors.

Maria R Aburto, Marta Magariños, Yolanda Leon, Isabel Varela-Nieto, Hortensia Sanchez-Calderon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
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  9. Stem Cell-Based Therapies in Hearing Loss.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Extraoral Taste Receptor Discovery: New Light on Ayurvedic Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2017
    Review
  19. Autophagy in the Vertebrate Inner Ear.Frontiers in cell and developmental biology · 2017
    Review
  20. 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

5 authors at 3 institutions in 1 country.

Maria R AburtoInstituto de Investigaciones Biomedicas Alberto Sols, CSIC-UAM, Madrid, Spain.
Marta Magariños
Yolanda Leon
Isabel Varela-Nieto
Hortensia Sanchez-Calderon
Instituto de Investigaciones Biomédicas Sols-Morreale · ESUniversidad Autónoma de Madrid · ESCentre for Biomedical Network Research on Rare Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOtic neurons and sensory cells derive from common progenitors whose transition into mature cells requires the coordination of cell survival, proliferation and differentiation programmes. Neurotrophic support and survival of post-mitotic otic neurons have been intensively studied, but the bases underlying the regulation of programmed cell death in immature proliferative otic neuroblasts remains poorly understood. The protein kinase AKT acts as a node, playing a critical role in controlling cell survival and cell cycle progression. AKT is activated by trophic factors, including insulin-like growth factor I (IGF-I), through the generation of the lipidic second messenger phosphatidylinositol 3-phosphate by phosphatidylinositol 3-kinase (PI3K). Here we have investigated the role of IGF-dependent activation of the PI3K-AKT pathway in maintenance of otic neuroblasts. METHODOLOGY/PRINCIPAL

findingsBy using a combination of organotypic cultures of chicken (Gallus gallus) otic vesicles and acoustic-vestibular ganglia, Western blotting, immunohistochemistry and in situ hybridization, we show that IGF-I-activation of AKT protects neural progenitors from programmed cell death. IGF-I maintains otic neuroblasts in an undifferentiated and proliferative state, which is characterised by the upregulation of the forkhead box M1 (FoxM1) transcription factor. By contrast, our results indicate that post-mitotic p27(Kip)-positive neurons become IGF-I independent as they extend their neuronal processes. Neurons gradually reduce their expression of the Igf1r, while they increase that of the neurotrophin receptor, TrkC. CONCLUSIONS/SIGNIFICANCE: Proliferative otic neuroblasts are dependent on the activation of the PI3K-AKT pathway by IGF-I for survival during the otic neuronal progenitor phase of early inner ear development.

Indexed as

AnimalsCaspase 3Cell ProliferationCells, CulturedCell SurvivalChick EmbryoEar, InnerGene Expression Regulation, DevelopmentalInsulin-Like Growth Factor IModels, BiologicalNeural Stem CellsNeuronsOncogene Protein v-aktPhosphatidylinositol 3-KinasesSignal TransductionTime FactorsCaspase 3Insulin-Like Growth Factor IOncogene Protein v-aktPhosphatidylinositol 3-Kinases

Identifiers

PMID22292041
PMCPMC3264639
OpenAlexW2050455948

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.