Evidence map›Paper›PMID 17084035›Full record

ArticleNeuroscience2006

Anti-apoptotic effect of granulocyte-colony stimulating factor after focal cerebral ischemia in the rat.

I Solaroglu, T Tsubokawa, J Cahill, J H Zhang

Abstract read
In one paragraph

Article in Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–field-weighted citation impact
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

66 citing papers in PubMed.

  1. Article
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  16. Hydroxy-Oxidative medicine and cellular longevity · 2020
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  18. Antiepileptic Effects of Protein-Rich Extract fromOxidative medicine and cellular longevity · 2019
    Article
  19. Effect of docosahexaenoic acid on traumatic brain injury in rats.Experimental and therapeutic medicine · 2017
    Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

4 authors.

I SolarogluDepartment of Physiology and Pharmacology, Loma Linda University, School of Medicine, Loma Linda, CA, USA.
T Tsubokawa
J Cahill
J H Zhang

Funding

Mechanisms of Hyperbaric Oxygen Induced Brain ProtectionR01NS043338 · NINDS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ZHANG, JOHN H · 2004 to 2014
$3.0M
Neurovascular Protection for Subarachnoid HemorrhageR01NS053407 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2006 to 2010
$1.8M
Oxygen Therapy in Neonatal Hypoxia-IschemiaR01HD043120 · NICHD · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ZHANG, JOHN H. · 2003 to 2007
$1.6M
Anti-apoptosis as a new therapy for cerebral vasospasmR01NS045694 · NINDS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ZHANG, JOHN H. · 2002 to 2005
$1.1M
NICHD NIH HHS HD43120NICHD NIH HHS R01 HD043120NINDS NIH HHS NS43338NINDS NIH HHS NS45694NINDS NIH HHS NS53407NINDS NIH HHS R01 NS043338NINDS NIH HHS R01 NS045694NINDS NIH HHS R01 NS053407
6 · The paper itself

Abstract

We investigated the molecular mechanisms of the anti-apoptotic properties of granulocyte-colony stimulating factor (G-CSF) on neurons and whether G-CSF affects glial cell survival following focal cerebral ischemia in rats. Sprague-Dawley rats were subjected to a transient 90 min middle cerebral artery occlusion (MCAO) by the intraluminal occlusion technique. Rats were treated with either a single dose of G-CSF (50 microg/kg, s.c.) at the onset of reperfusion or G-CSF (50 microg/kg body weight, s.c.) was administered starting at the onset of reperfusion and followed by the administration of the same dose per day for an additional 2 days. Brains were harvested either 24 h, 72 h or 2 weeks after reperfusion for assays of infarct volume, immunohistological studies and Western blot analysis for phosphorylated signal transducer and activator of transcription 3 (pSTAT3), Pim-1, bcl-2, Bax, cytochrome c, cellular inhibitor of apoptosis protein 2 (cIAP2), and cleaved caspase-3 levels. G-CSF significantly reduced infarct volume and ameliorated the early neurological outcome. G-CSF treatment significantly up-regulated pSTAT3, Pim-1, bcl-2 expression, and down-regulated cytochrome c release to the cytosol, Bax translocation to the mitochondria, and cleaved caspase-3 levels in neurons. The activation of the STAT3 pathway was accompanied by increased cIAP2 expression in glial cells. After MCAO, G-CSF treatment increased both neuronal and glial survival by effecting different anti-apoptotic pathways which reflects the multifactorial actions of this drug. These changes were associated with remarkable improvement in tissue preservation and behavioral outcome.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBrain IschemiaCell SurvivalCerebral InfarctionDisease Models, AnimalDown-RegulationDrug Administration ScheduleGranulocyte Colony-Stimulating FactorInfarction, Middle Cerebral ArteryMaleNeurogliaNeuronsNeuroprotective AgentsProtein TransportApoptosis Regulatory ProteinsGranulocyte Colony-Stimulating FactorNeuroprotective Agents

Identifiers

PMID17084035
PMCPMC1820637

What OpenQuestion holds

Textmetadata
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.