Abstract

Two types of reactive astrocytes, A1 and A2 astrocytes, are induced following neuroinflammation and ischemia. In this study, we evaluated the effects of the fibroblast growth factor (FGF)2/FGF receptor (FGFR)1 pathway on A1 and A2 astrocytes in the rat hippocampus using double-labeling immunofluorescence following infrasound exposure. A1 astrocytes were induced in the CA1 region of the hippocampus after exposure to infrasound for 3 days. The number of microglial cells was also increased, and we investigated if these might be responsible for the reactivity of A1 astrocytes. Accordingly, expression levels of C3 and Iba-1, as markers of A1 astrocytes and microglial cells, respectively, were both up-regulated in rat hippocampus following infrasound exposure, as demonstrated by western blot. We also explored the effect of the FGF2/FGFR1 pathway on A1 astrocyte reactivity by pretreating rats with FGF2 or the specific FGFR1 antagonist, PD173074. A1 astrocytes were gradually down-regulated by activation of the FGF2/FGFR1 pathway and were up-regulated by inhibition of the FGF2/FGFR1 pathway after infrasound damage. These results further our understanding of the role of reactive astrocytes in infrasound-induced central nervous system injury and will thus facilitate the development of new treatments for these injuries.

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  • We previously showed that the fibroblast growth factor (FGF)2/FGF receptor (FGFR)1 pathway inhibited astrocytemediated neuroinflammation in vitro and in vivo after infrasound exposure (Shi et al, 2018), suggesting that the reactivity of A1 astrocytes was related to activation of this pathway

  • We previously demonstrated that infrasound exposure induced astrocyte and microglial activation (Shi et al, 2013; Cai et al, 2014)

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Summary

Introduction

Infrasound is generated by numerous environmental factors, including agricultural machinery and industrial processes (Backteman et al, 1983; Bilski, 2017), and has been implicated in various kinds of health damage. Human and animal experiments have suggested that prolonged infrasound exposure can damage the central nervous system (CNS), including the hippocampus, cerebellum, limbic-corticular complex, hypothalamus, and cortex (Izmerov et al, 1997; Fei et al, 2000; Yuan et al, 2009; Shi et al, 2013; Cai et al, 2014; Ma et al, 2015). We previously confirmed that infrasound exposure activated astrocytes and induced neuronal apoptosis in the CNS, which subsequently impaired spatial learning and memory abilities (Shi et al, 2013, 2018).

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