Glia maturation factor-β: a potential therapeutic target in neurodegeneration and neuroinflammation

Figures & data

Figure 1 Possible signaling pathways of GMFB.

Notes: (A) Expression of GMFB in the astrocytes may lead to the activation of p38 MAPK, and subsequently the activation of NF-κB, and finally the expression of GM-CSF. Increased secretion of GM-CSF by the astrocytes may stimulate the microglia and result in the overexpression of some pro-inflammatory cytokines/chemokines. (B) Expression of GMFB in the astrocytes may lead to the activation of p38 MAPK, and subsequently the activation of NF-κB, and finally the expression of Cu-Zn SOD. Increased expression of Cu-Zn SOD may lead to the overproduction of H₂O₂; H₂O₂ can in turn promote the activation of both p38 MAPK and NF-κB, thus forming a vicious cycle of oxidative stress. (C) Expression of GMFB in the astrocytes may lead to the activation of p38 and ERK MAPKs, and subsequently the activation of transcription factors, and finally stimulate the expression of some neurotrophins. (D) GMFB overexpression may activate GSK-3β and caspase-3 and promote apoptosis.
Abbreviations: BDNF, brain-derived neurotrophic factor; CREB, cAMP responsive element binding protein; Cu-Zn SOD, copper–zinc superoxide dismutase; ERK, extracellular signal-regulated kinase; GM-CSF, granulocyte-macrophage colony-stimulating factor; GMFB, glia maturation factor-β; GSK-3β, glycogen synthase kinase-3β; H₂O₂, hydrogen peroxide; IFN, interferon; IL, interleukin; IP-10, interferon-γ-inducible 10 kDa protein; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB; NGF, nerve growth factor; TNF, tumor necrosis factor.