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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...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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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. |
format | Online Article Text |
id | pubmed-4730282 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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