Evidence map›Paper›PMID 19526277›Full record

ArticleNeurotoxicity research2009

IGF-1 and pAKT signaling promote hippocampal CA1 neuronal survival following injury to dentate granule cells.

Robert N Wine, Christopher A McPherson, G Jean Harry

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Immunological biomarkers of aging.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Toxin-Induced Experimental Models of Learning and Memory Impairment.International journal of molecular sciences · 2016
    Review
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Robert N WineLaboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, P.O. Box 12233, MD C1-04, Research Triangle Park, NC 27709, USA.
Christopher A McPherson
G Jean Harry
National Institutes of Health · US

Funding

Environmentally Induced Alterations In Neuron And Glia Development and AgingZIAES021164 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HARRY, GAYLIA JEAN · 2009 to 2021
$15.4M
Neuroimmunotoxicology: autoimmunity, inflammation, age, environmental agentsZIAES101623 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HARRY, GAYLIA JEAN · 2009 to 2012
$1.7M
Intramural NIH HHS ZIA ES101623
6 · The paper itself

Abstract

Insulin-like growth factor-1 (IGF-1) protects neurons from apoptosis and in vivo offers neuroprotective support to hippocampal CA1 pyramidal neurons following ischemia or seizure. IGF-1 signals through IGF-1 receptors activating phosphytidylinositol 3-kinase (PI3K)/Akt or pMAPK pathways. IGF-1 can be induced with injury and microglia and astrocytes may serve as a source of this neurotrophic factor to promote neuronal survival. An acute systemic injection of trimethyltin (TMT; 2 mg/kg, ip) to mice induces apoptosis of dentate granule neurons within 24 h and a differential response of microglia with ramified microglia present in the CA-1 region. Using this model, we studied the role of IGF-1 in the survival of CA-1 pyramidal neurons under conditions of altered synaptic input due to changes in the dentate gyrus. Within 24 h of injection, IGF-1 mRNA levels were elevated in the hippocampus and IGF-1 protein detected in both astrocytes and microglia. IGF-1 was redistributed within the CA-1 neurons corresponding with an increase in cytoplasmic pAkt, elevated PKBalpha/Akt protein levels, and a decrease in the antagonist, Rho. pMAPK was not detected in CA-1 neurons and ERK2 showed a transient decrease followed by a significant increase, suggesting a lack of recruitment of the pMAPK signaling pathway for neuronal survival. In mice deficient for IGF-1, a similar level of apoptosis was observed in dentate granule neurons as compared to wildtype; however, TMT induced a significant level CA-1 neuronal death, further supporting a role for IGF-1 in the survival of CA-1 neurons.

Indexed as

AnimalsAnimals, NewbornBrain InjuriesCA1 Region, HippocampalCaspase 3Dentate GyrusDisease Models, AnimalFluoresceinsGene Expression RegulationGlial Fibrillary Acidic ProteinGlycoproteinsInsulin-Like Growth Factor IMiceMice, KnockoutMicrogliaMitogen-Activated Protein Kinase KinasesCaspase 3Fluoresceinsfluoro jadeGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseGlycoproteinsInsulin-Like Growth Factor Iisolectin B4-binding glycoprotein, mouseMitogen-Activated Protein Kinase KinasesNerve Tissue ProteinsOncogene Protein v-aktOrganic ChemicalsTrimethyltin Compoundstrimethyltin hydroxide

Identifiers

PMID19526277
PMCPMC6276784
OpenAlexW2048069434

What OpenQuestion holds

Textmetadata
LicenceTDM
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.