Evidence map›Paper›PMID 28575743›Full record

ArticleRedox biology2017

IGF-II promotes neuroprotection and neuroplasticity recovery in a long-lasting model of oxidative damage induced by glucocorticoids.

E Martín-Montañez, C Millon, F Boraldi, F Garcia-Guirado, C Pedraza, E Lara, L J Santin, J Pavia, M Garcia-Fernandez

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 80 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

E Martín-MontañezDepartment of Pharmacology and Paediatrics, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
C MillonDepartment of Human Physiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
F BoraldiDepartment of Life Sciences, University of Modena e Reggio Emilia, Modena, Italy.
F Garcia-GuiradoDepartment of Human Physiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
C PedrazaDepartment of Psychobiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
E LaraDepartment of Human Physiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
L J SantinDepartment of Psychobiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain.
J PaviaDepartment of Pharmacology and Paediatrics, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain. Electronic address: pavia@uma.es.
M Garcia-FernandezDepartment of Human Physiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain. Electronic address: igf@uma.es.
Instituto de Investigación Biomédica de Málaga · ESUniversidad de Málaga · ESUniversity of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor-II (IGF-II) is a naturally occurring hormone that exerts neurotrophic and neuroprotective properties in a wide range of neurodegenerative diseases and ageing. Accumulating evidence suggests that the effects of IGF-II in the brain may be explained by its binding to the specific transmembrane receptor, IGFII/M6P receptor (IGF-IIR). However, relatively little is known regarding the role of IGF-II through IGF-IIR in neuroprotection. Here, using adult cortical neuronal cultures, we investigated whether IGF-II exhibits long-term antioxidant effects and neuroprotection at the synaptic level after oxidative damage induced by high and transient levels of corticosterone (CORT). Furthermore, the involvement of the IGF-IIR was also studied to elucidate its role in the neuroprotective actions of IGF-II. We found that neurons treated with IGF-II after CORT incubation showed reduced oxidative stress damage and recovered antioxidant status (normalized total antioxidant status, lipid hydroperoxides and NAD(P) H:quinone oxidoreductase activity). Similar results were obtained when mitochondria function was analysed (cytochrome c oxidase activity, mitochondrial membrane potential and subcellular mitochondrial distribution). Furthermore, neuronal impairment and degeneration were also assessed (synaptophysin and PSD-95 expression, presynaptic function and FluoroJade B® stain). IGF-II was also able to recover the long-lasting neuronal cell damage. Finally, the effects of IGF-II were not blocked by an IGF-IR antagonist, suggesting the involvement of IGF-IIR. Altogether these results suggest that, in or model, IGF-II through IGF-IIR is able to revert the oxidative damage induced by CORT. In accordance with the neuroprotective role of the IGF-II/IGF-IIR reported in our study, pharmacotherapy approaches targeting this pathway may be useful for the treatment of diseases associated with cognitive deficits (i.e., neurodegenerative disorders, depression, etc.).

Indexed as

Neuronal PlasticityOxidative StressAnimalsCells, CulturedDisks Large Homolog 4 ProteinElectron Transport Complex IVGlucocorticoidsInsulin-Like Growth Factor IIMembrane Potential, MitochondrialNeuronsNeuroprotective AgentsRatsReceptor, IGF Type 2SynapsesSynaptophysinDisks Large Homolog 4 ProteinElectron Transport Complex IVGlucocorticoidsInsulin-Like Growth Factor IINeuroprotective AgentsReceptor, IGF Type 2SynaptophysinInsulin-like growth factor-IIInsulin-like growth factor-II receptorMitochondriaNeuroprotectionOxidative stressSynapsis

Identifiers

PMID28575743
PMCPMC5454142
OpenAlexW2619912632

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.