GM-CSF inhibits apoptosis of neural cells via regulating the expression of apoptosis-related proteins

Huang, Xian; Choi, Jung Kyoung; Park, Sora; Ha, Yoon; Park, Hyeonseon; Yoon, Seung Hwan; Park, Hyung Chun; Park, Jong Oon; Choi, Byung Hyune

doi:10.1016/j.neures.2007.01.015

Cited by 59 publications

(67 citation statements)

References 26 publications

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“…There was no significant difference in cleavage rate between the two groups, but cloned embryos in the presence of pGM-CSF had a tendency (P=0.06) to have more 4-5-cell stage embryos. This may have been due to its cytoprotective effects [20] in preimplantation embryos when they are cultured with pGM-CSF in early developmental stages. Improved development of cloned embryos in the presence of pGM-CSF implies that the effect of GM-CSF is not limited to parthenogenetic or in vitro-fertilized embryos only.…”

Section: Discussionmentioning

confidence: 99%

Porcine Granulocyte-Macrophage Colony-Stimulating Factor Improves the <i>in vitro</i> Development of Cloned Porcine Embryos

Kwak

Cheong

Jeon

et al. 2012

The Journal of Veterinary Medical Science

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ABSTRACT. We examined the effects of porcine granulocyte-macrophage colony-stimulating factor (pGM-CSF) on the in vitro development of porcine embryos produced by somatic cell nuclear transfer (SCNT) for the first time. We evaluated the effects of pGM-CSF on SCNTderived blastocyst formation and investigated gene expression. A total of 522 cloned embryos in 6 replicates were treated with 10 ng/ml pGM-CSF during in vitro culture (IVC). This treatment significantly (P<0.05) increased blastocyst formation and total cell number in blastocysts compared with the control (12.3% and 41.4 vs. 9.0% and 34.7, respectively). However, there was no effect on cleavage rate. The numbers of cells in the inner cell mass and trophectoderm were significantly higher in the pGM-CSF treatment group (6.0 and 43.0, respectively) compared with the control (4.4 and 31.9, respectively). Treatment with 10 ng/ml pGM-CSF significantly increased POU5F1 and Cdx2 mRNA expression in blastocysts. In addition, Bcl-2, Dnmt1 and proliferating cell nuclear antigen (PCNA) mRNA expression were upregulated in blastocysts in the pGM-CSF supplemented group compared with the control. These results suggest that pGM-CSF improves the quality and developmental viability of porcine SCNT embryos by regulating transcription factor expression.

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Section: Discussionmentioning

confidence: 99%

Porcine Granulocyte-Macrophage Colony-Stimulating Factor Improves the <i>in vitro</i> Development of Cloned Porcine Embryos

Kwak

Cheong

Jeon

et al. 2012

The Journal of Veterinary Medical Science

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“…10 GM-CSF is neuroprotective after a wide range of neurotrauma, exerting neuroprotective effects by diminishing expression of apoptosis-related genes. [11][12][13][14][15] …”

Section: Normal Brain Tissue Synthesizes G(m)-csfmentioning

confidence: 99%

Glioblastoma-synthesized G-CSF and GM-CSF contribute to growth and immunosuppression: Potential therapeutic benefit from dapsone, fenofibrate, and ribavirin

Kast¹,

Hill

Wion

et al. 2017

Tumour Biol.

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Increased ratio of circulating neutrophils to lymphocytes is a common finding in glioblastoma and other cancers. Data reviewed establish that any damage to brain tissue tends to cause an increase in G-CSF and/or GM-CSF (G(M)-CSF) synthesized by the brain. Glioblastoma cells themselves also synthesize G(M)-CSF. G(M)-CSF synthesized by brain due to damage by a growing tumor and by the tumor itself stimulates bone marrow to shift hematopoiesis toward granulocytic lineages away from lymphocytic lineages. This shift is immunosuppressive and generates the relative lymphopenia characteristic of glioblastoma. Any trauma to brain-be it blunt, sharp, ischemic, infectious, cytotoxic, tumor encroachment, or radiation-increases brain synthesis of G(M)-CSF. G(M)-CSF are growth and motility enhancing factors for glioblastomas. High levels of G(M)-CSF contribute to the characteristic neutrophilia and lymphopenia of glioblastoma. Hematopoietic bone marrow becomes entrained with, directed by, and contributes to glioblastoma pathology. The antibiotic dapsone, the lipid-lowering agent fenofibrate, and the antiviral drug ribavirin are Food and Drug Administration-and European Medicines Agency-approved medicines that have potential to lower synthesis or effects of G(M)-CSF and thus deprive a glioblastoma of some of the growth promoting contributions of bone marrow and G(M)-CSF.

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“…The improvement is probably due to the prevention of apoptosis of the cells, including neurons,46 via reduction of the expression of the proapoptotic proteins p53, p21, and Bax, and induction of nucleophosmin‐144 and the antiapoptotic protein B‐cell lymphoma 2 (Bcl‐2) 45. Additionally, GM‐CSF increased BDNF expression by macrophages, and subsequently stimulated axonal regeneration 49.…”

Section: Roles Of Inflammatory Cytokines In Sci Repairmentioning

confidence: 99%

“…After SCI, topically implanted gelfoam sponges soaked with IL‐12 increased the number of activated ameboid‐type microglia/macrophages and their BDNF expression, accompanied by increased remyelination and promotion of functional recovery 75. In another study, gelfoam sponges loaded with GM‐CSF modulated apoptosis and promoted neuroprotection 179. Further, Li et al developed an NT‐3/fibroin‐coated gelatin sponge scaffold, which could continually release NT‐3 for 28 days 180.…”

Section: Local Delivery Of Therapeutic Agents Regulates Inflammatory mentioning

confidence: 99%

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

et al. 2018

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The balance of inflammation is critical to the repair of spinal cord injury (SCI), which is one of the most devastating traumas in human beings. Inflammatory cytokines, the direct mediators of local inflammation, have differential influences on the repair of the injured spinal cord. Some inflammatory cytokines are demonstrated beneficial to spinal cord repair in SCI models, while some detrimental. Various animal researches have revealed that local delivery of therapeutic agents efficiently regulates inflammatory cytokines and promotes repair from SCI. Quite a few clinical studies have also shown the promotion of repair from SCI through regulation of inflammatory cytokines. However, local delivery of a single agent affects only a part of the inflammatory cytokines that need to be regulated. Meanwhile, different individuals have differential profiles of inflammatory cytokines. Therefore, future studies may aim to develop personalized strategies of locally delivered therapeutic agent cocktails for effective and precise regulation of inflammation, and substantial functional recovery from SCI.

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GM-CSF inhibits apoptosis of neural cells via regulating the expression of apoptosis-related proteins

Cited by 59 publications

References 26 publications

Porcine Granulocyte-Macrophage Colony-Stimulating Factor Improves the <i>in vitro</i> Development of Cloned Porcine Embryos

Porcine Granulocyte-Macrophage Colony-Stimulating Factor Improves the <i>in vitro</i> Development of Cloned Porcine Embryos

Glioblastoma-synthesized G-CSF and GM-CSF contribute to growth and immunosuppression: Potential therapeutic benefit from dapsone, fenofibrate, and ribavirin

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

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