TY - JOUR
T1 - The role of TNF-alpha and its receptors in the production of NGF and GDNF by astrocytes
AU - Kuno, Reiko
AU - Yoshida, Yusuke
AU - Nitta, Atsumi
AU - Nabeshima, Toshitaka
AU - Wang, Jinyan
AU - Sonobe, Yoshifumi
AU - Kawanokuchi, Jun
AU - Takeuchi, Hideyuki
AU - Mizuno, Tetsuya
AU - Suzumura, Akio
N1 - Funding Information:
This work was supported in part by the Neuroimmunological Disease Research Committee grant from the Ministry of Health, Labour, and Welfare of Japan, and a Grant-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology. This work was also supported by the 21st COE Program “Integrated Molecular Medicine for Neuronal and Neoplastic Disorders” from the Ministry of Education, Culture, Sports, Science, and Technology.
PY - 2006/10/20
Y1 - 2006/10/20
N2 - The neurotrophic factors, nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF), are produced by astrocytes, and are induced by inflammatory stimuli including bacterial lipopolysaccharide and pro-inflammatory cytokines. In this study, we examined the regulatory mechanisms of tumor necrosis factor-α (TNF-α)-induced production of neurotrophic factors. We show here that cultured astrocytes express both TNF-α receptor 1 (TNFR1) and TNFR2, and that activation of these receptors by TNF-α promotes expression of both NGF and GDNF. In addition, we observe that not only exogenous TNF-α but also TNF-α produced by astrocytes induce NGF and GDNF production in astrocytes. These results suggest that an autocrine loop involving TNF-α contributes to the production of neurotrophic factors in response to inflammation.
AB - The neurotrophic factors, nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF), are produced by astrocytes, and are induced by inflammatory stimuli including bacterial lipopolysaccharide and pro-inflammatory cytokines. In this study, we examined the regulatory mechanisms of tumor necrosis factor-α (TNF-α)-induced production of neurotrophic factors. We show here that cultured astrocytes express both TNF-α receptor 1 (TNFR1) and TNFR2, and that activation of these receptors by TNF-α promotes expression of both NGF and GDNF. In addition, we observe that not only exogenous TNF-α but also TNF-α produced by astrocytes induce NGF and GDNF production in astrocytes. These results suggest that an autocrine loop involving TNF-α contributes to the production of neurotrophic factors in response to inflammation.
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U2 - 10.1016/j.brainres.2006.07.120
DO - 10.1016/j.brainres.2006.07.120
M3 - Article
C2 - 16956589
AN - SCOPUS:33749246536
SN - 0006-8993
VL - 1116
SP - 12
EP - 18
JO - Brain Research
JF - Brain Research
IS - 1
ER -