We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Protection of granulocyte-colony stimulating factor to hemorrhagic brain injuries and its involved mechanisms: effects of vascular endothelial growth factor and aquaporin-4.
Neuroscience 2014 Februrary 29
Granulocyte-colony stimulating factor (G-CSF) has protective effects on many neurological diseases. Here, we aimed to test G-CSF's effects on perihematomal tissue injuries following intracerebral hemorrhage (ICH) and examine whether the effects were functionally dependent on vascular endothelial growth factor (VEGF) and aquaporin-4 (AQP4). We detected the expression of perihematomal VEGF, VEGF receptors (VEGFRs) and AQP4 at 1, 3 and 7days after ICH. Also, we examined the effects of G-CSF on tissue injuries by ICH in wild type mice, and tested whether such effects were VEGF and AQP4 dependent by using VEGFR inhibitor - SU5416 and AQP4 knock-out (AQP4(-/-)) mice. Furthermore, we assessed the related signal transduction pathways via astrocyte cultures. We found G-CSF highly increased perihematomal VEGF, VEGFR-2 and AQP4. Importantly, G-CSF led to neurological functional improvement in both types of mice by associating with reduction of brain edema, blood-brain barrier (BBB) permeability and neuronal death and apoptosis and statistical analysis suggested AQP4 was required for these effects. Besides, except BBB leakage alleviation, the above effects were attenuated but not counteracted by SU5416, suggesting involvement of VEGF. G-CSF up-regulated phosphorylation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3) as well as VEGF and AQP4 proteins in cultured astrocytes. The latter was inhibited by ERK and STAT3 inhibitors respectively. Our data suggest the protective effects of G-CSF on perihematomal tissue injuries after ICH are highly associated with the increased levels of VEGF and AQP4, possibly act through C-Jun amino-terminal kinase and ERK pathways respectively.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app