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Int. J. Mol. Sci. 2016, 17(1), 37; doi:10.3390/ijms17010037

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

1
Key Laboratory of Biotechnology and Pharmaceutical Engineering, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China
2
Department of Pharmacy, Ningbo Medical Treatment Center, Li Huili Hospital, Ningbo 315040, China
3
Emergency Department, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China
4
Department of Neurosurgery, Cixi People’s Hospital, Wenzhou Medical University, Cixi, Ningbo 315300, China
5
Department of Gastroenterology, Ningbo Medical Treatment Center Li Huili Hospital, Ningbo 315040, China
6
Department of Orthopaedics, the Second Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Alan C. Leonard
Received: 26 November 2015 / Revised: 23 December 2015 / Accepted: 24 December 2015 / Published: 28 December 2015
(This article belongs to the Special Issue Molecular Machinery of Cell Growth Regulation)
View Full-Text   |   Download PDF [4472 KB, uploaded 28 December 2015]   |  

Abstract

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. View Full-Text
Keywords: astrocytes; bFGF; TLR4/NFκB; GFAP; vimentin astrocytes; bFGF; TLR4/NFκB; GFAP; vimentin
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Ye, L.; Yang, Y.; Zhang, X.; Cai, P.; Li, R.; Chen, D.; Wei, X.; Zhang, X.; Xu, H.; Xiao, J.; Li, X.; Lin, L.; Zhang, H. The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals. Int. J. Mol. Sci. 2016, 17, 37.

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