Evidence map›Paper›PMID 28420864›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Insulin Growth Factor 1 Protects Neural Stem Cells Against Apoptosis Induced by Hypoxia Through Akt/Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase (Akt/MAPK/ERK) Pathway in Hypoxia-Ishchemic Encephalopathy.

Bing Zhao, Zebao Zheng

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
7.7field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

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  16. Evaluation of Hypoxia on the Expression of miR-646/IGF-1 Signaling in Human Periodontal Ligament Cells (hPDLCs).Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Relationship Between INPP5E Gene Expression and Embryonic Neural Development in a Mouse Model of Neural Tube Defect.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Bing ZhaoDepartment of Children Rehabilitation, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Zebao ZhengDepartment of Children Rehabilitation, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Jining First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Insulin growth factor 1 (IGF-1) is reported to modulate cell growth and acts as potential therapy for traumatic brain injury. This study was designed to investigate the effect of IGF-1 on hypoxia-induced apoptosis in neural stem cells (NSCs). MATERIAL AND METHODS A hypoxia model was constructed using NSCs separated from the hippocampus of rat. NSCs were divided into four groups: cells under normoxic conditions that acted as controls (C group), cells under hypoxia (H group), cells under hypoxia with IGF-1 (HI group), and cells under hypoxia with IGF-1 as well as picropodophyllin (PPP), which acts as an inhibitor of the IGF-1 receptor (HIP group). The cell viability and apoptosis were respectively measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Finally, the phosphorylation levels of apoptosis-associated proteins and key kinases in the phosphatidylinositol-3-kinase (PI3K)/AKT and the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways were detected by Western blot analysis. RESULTS In comparison with the H group, the cell viability was increased while the cell apoptosis was reduced by IGF-1 in the HI group. Besides, the expression levels of Bax, cytochrome c, and activated caspase-3 were all improved in the H group, and the remarkable differences were eliminated in the HI group compared with the C group. The expression level of Bcl-2 was the opposite. Additionally, down-regulations of phosphorylated AKT, MAPK, and ERK induced by hypoxia were all improved by IGF-1. All the influences of IGF-1 were weakened by addition of PPP. CONCLUSIONS IGF-1 increased cell viability while decreasing apoptosis in hypoxic NSCs through the PI3K/AKT and MAPK/ERK pathways.

Indexed as

AnimalsApoptosisCell CycleCell HypoxiaCell ProliferationCell SurvivalDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesHippocampusHypoxia-Ischemia, BrainInsulin-Like Growth Factor IMAP Kinase Signaling SystemNeural Stem CellsPhosphatidylinositol 3-KinasesPhosphorylationPodophyllotoxinExtracellular Signal-Regulated MAP KinasesInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasespicropodophyllinPodophyllotoxinProtective AgentsProto-Oncogene Proteins c-akt

Identifiers

PMID28420864
PMCPMC5405785
OpenAlexW2606444637

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.