ArticleMolecular neurobiology2014
Granulocyte macrophage colony-stimulating factor shows anti-apoptotic activity via the PI3K-NF-κB-HIF-1α-survivin pathway in mouse neural progenitor cells.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- IFN-γ-independent control of M. tuberculosis requires CD4 T cell-derived GM-CSF and activation of HIF-1α.PLoS pathogens · 2022Article
- The innate immune system stimulating cytokine GM-CSF improves learning/memory and interneuron and astrocyte brain pathology in Dp16 Down syndrome mice and improves learning/memory in wild-type mice.Neurobiology of disease · 2022Article
- Article
- Circular RNA circIKBKB promotes breast cancer bone metastasis through sustaining NF-κB/bone remodeling factors signaling.Molecular cancer · 2021Article
- Overlapping migratory mechanisms between neural progenitor cells and brain tumor stem cells.Cellular and molecular life sciences : CMLS · 2019Review
- The antidepressant effects of GM-CSF are mediated by the reduction of TLR4/NF-ĸB-induced IDO expression.Journal of neuroinflammation · 2019Article
- Overexpression of caudal type homeobox transcription factor 2 inhibits the growth of the MGC-803 human gastric cancer cell line in vivo.Molecular medicine reports · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulocyte macrophage-colony stimulating factor (GM-CSF) is a hematopoietic cytokine that plays a crucial role in regulating the proliferation, differentiation, and survival of hematopoietic cells. Recent studies have shown that GM-CSF also has anti-apoptotic effects and regulates the expression of anti-apoptotic genes including Bcl-2 family proteins in neuronal cells in vitro and in vivo. However, the mechanism underlying the anti-apoptotic function of GM-CSF is not well understood. In the present work, we examined the role of phosphoinositide 3-kinase (PI3K)-AKT signal pathway in the anti-apoptotic activity of GM-CSF in mouse neural progenitor cells (NPCs). In terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, the anti-apoptotic effect of GM-CSF (apoptotic population of approximately 8.17 %) on staurosporine-induced apoptosis of NPCs (31.09 %) was significantly blocked by LY294002, an inhibitor of PI3K signal (24.04 %). We found that the PI3K-AKT signal pathway induced by GM-CSF treatment activated nuclear factor κB (NF-κB) and increased the expression of hypoxia-inducible factor 1α (HIF-1α) in normoxic conditions. Analyses using specific small interfering RNAs (siRNAs) showed that NF-κB was an upstream molecule of HIF-1α and activated its expression at the mRNA level. Further analyses using the siRNAs and chromatin immunoprecipitation (ChIP) showed that HIF-1α was responsible for the induced expression of survivin, a member of the inhibitor of apoptosis proteins (IAPs). Each of the specific siRNAs for NF-κB, HIF-1α, and survivin inhibited significantly the anti-apoptotic activity of GM-CSF on the staurosporine-induced apoptosis in NPCs in TUNEL assays. The results of this study showed the downstream signals and mechanism of PI3K/AKT-mediated anti-apoptotic activity of GM-CSF in NPCs, particularly revealing the role of the NF-κB-HIF-1α-survivin cascade.
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