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The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals

Astrocytes have critical roles in immune defense, homeostasis, metabolism, and synaptic remodeling and function in the central nervous system (CNS); however, excessive activation of astrocytes with increased intermediate filaments following neuronal trauma, infection, ischemia, stroke, and neurodege...

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Autores principales: Ye, Libing, Yang, Ying, Zhang, Xie, Cai, Pingtao, Li, Rui, Chen, Daqing, Wei, Xiaojie, Zhang, Xuesong, Xu, Huazi, Xiao, Jian, Li, Xiaokun, Lin, Li, Zhang, Hongyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730282/
https://www.ncbi.nlm.nih.gov/pubmed/26729092
http://dx.doi.org/10.3390/ijms17010037
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author Ye, Libing
Yang, Ying
Zhang, Xie
Cai, Pingtao
Li, Rui
Chen, Daqing
Wei, Xiaojie
Zhang, Xuesong
Xu, Huazi
Xiao, Jian
Li, Xiaokun
Lin, Li
Zhang, Hongyu
author_facet Ye, Libing
Yang, Ying
Zhang, Xie
Cai, Pingtao
Li, Rui
Chen, Daqing
Wei, Xiaojie
Zhang, Xuesong
Xu, Huazi
Xiao, Jian
Li, Xiaokun
Lin, Li
Zhang, Hongyu
author_sort Ye, Libing
collection PubMed
description Astrocytes have critical roles in immune defense, homeostasis, metabolism, and synaptic remodeling and function in the central nervous system (CNS); however, excessive activation of astrocytes with increased intermediate filaments following neuronal trauma, infection, ischemia, stroke, and neurodegenerative diseases results in a pro-inflammatory environment and promotes neuronal death. As an important neurotrophic factor, the secretion of endogenous basic fibroblast growth factor (bFGF) contributes to the protective effect of neuronal cells, but the mechanism of bFGF in reactive astrogliosis is still unclear. In this study, we demonstrated that exogenous bFGF attenuated astrocyte activation by reducing the expression of glial fibrillary acidic protein (GFAP) and other markers, including neurocan and vimentin, but not nestin and decreased the levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), via the regulation of the upstream toll-like receptor 4/nuclear factor κB (TLR4/NFκB) signaling pathway. Our study suggests that the function of bFGF is not only related to the neuroprotective and neurotrophic effect but also involved in the inhibition of excessive astrogliosis and glial scarring after neuronal injury.
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spelling pubmed-47302822016-02-11 The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals Ye, Libing Yang, Ying Zhang, Xie Cai, Pingtao Li, Rui Chen, Daqing Wei, Xiaojie Zhang, Xuesong Xu, Huazi Xiao, Jian Li, Xiaokun Lin, Li Zhang, Hongyu Int J Mol Sci Article Astrocytes have critical roles in immune defense, homeostasis, metabolism, and synaptic remodeling and function in the central nervous system (CNS); however, excessive activation of astrocytes with increased intermediate filaments following neuronal trauma, infection, ischemia, stroke, and neurodegenerative diseases results in a pro-inflammatory environment and promotes neuronal death. As an important neurotrophic factor, the secretion of endogenous basic fibroblast growth factor (bFGF) contributes to the protective effect of neuronal cells, but the mechanism of bFGF in reactive astrogliosis is still unclear. In this study, we demonstrated that exogenous bFGF attenuated astrocyte activation by reducing the expression of glial fibrillary acidic protein (GFAP) and other markers, including neurocan and vimentin, but not nestin and decreased the levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), via the regulation of the upstream toll-like receptor 4/nuclear factor κB (TLR4/NFκB) signaling pathway. Our study suggests that the function of bFGF is not only related to the neuroprotective and neurotrophic effect but also involved in the inhibition of excessive astrogliosis and glial scarring after neuronal injury. MDPI 2015-12-28 /pmc/articles/PMC4730282/ /pubmed/26729092 http://dx.doi.org/10.3390/ijms17010037 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Ye, Libing
Yang, Ying
Zhang, Xie
Cai, Pingtao
Li, Rui
Chen, Daqing
Wei, Xiaojie
Zhang, Xuesong
Xu, Huazi
Xiao, Jian
Li, Xiaokun
Lin, Li
Zhang, Hongyu
The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title_full The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title_fullStr The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title_full_unstemmed The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title_short The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals
title_sort role of bfgf in the excessive activation of astrocytes is related to the inhibition of tlr4/nfκb signals
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730282/
https://www.ncbi.nlm.nih.gov/pubmed/26729092
http://dx.doi.org/10.3390/ijms17010037
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