Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells

Abstract Our previous studies have shown adenosine A2A R activation markedly promotes the expression of cystatin F (CF) and exacerbates the white matter lesions induced by hypoxic brain injuries. Thus, we hypothesized that CF was probably involved in neuroinflammation of activated microglia induced...

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Autores principales:	Wei Duan, Haoxiang Wang, Qinlin Fan, Lin Chen, Heqing Huang, Hong Ran
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ae788e8298ef4a87975a562c4edcab2c
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spelling	oai:doaj.org-article:ae788e8298ef4a87975a562c4edcab2c2021-12-02T16:07:50ZCystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells10.1038/s41598-018-25031-52045-2322https://doaj.org/article/ae788e8298ef4a87975a562c4edcab2c2018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25031-5https://doaj.org/toc/2045-2322Abstract Our previous studies have shown adenosine A2A R activation markedly promotes the expression of cystatin F (CF) and exacerbates the white matter lesions induced by hypoxic brain injuries. Thus, we hypothesized that CF was probably involved in neuroinflammation of activated microglia induced by A2A R activation. We transfected the BV2 cells with a CF shRNA vector and examined the production of pro-inflammatory cytokines in hypoxic-BV2 cells in which A2A R was activated or inactivated to confirm this hypothesis. Additionally, we also investigated the probable signaling pathways involved in modulation of A2A R activation on CF expression in hypoxia-activated BV2 cells. Activation of A2A R promoted CF expression, which was significantly increased after the low glucose and hypoxia treatments in BV2 cells. CF gene knockdown markedly inhibited the increase in the expression of pro-inflammatory cytokines induced by A2A R activation in hypoxic-BV2 cells. Furthermore, the increased expression of the CF induced by A2A R activation was remarkably inhibited in hypoxic-BV2 cells administrated with the PKA inhibitor H-89 and the PKC inhibitor staurosporine. Hence, these results indicate that hypoxia BV2 cells highly express CF, which is involved in A2A R activation-mediated neuroinflammation via the PKA/CREB and PKC/CREB or ERK1/2 signaling pathways.Wei DuanHaoxiang WangQinlin FanLin ChenHeqing HuangHong RanNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-14 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Wei Duan Haoxiang Wang Qinlin Fan Lin Chen Heqing Huang Hong Ran Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
description	Abstract Our previous studies have shown adenosine A2A R activation markedly promotes the expression of cystatin F (CF) and exacerbates the white matter lesions induced by hypoxic brain injuries. Thus, we hypothesized that CF was probably involved in neuroinflammation of activated microglia induced by A2A R activation. We transfected the BV2 cells with a CF shRNA vector and examined the production of pro-inflammatory cytokines in hypoxic-BV2 cells in which A2A R was activated or inactivated to confirm this hypothesis. Additionally, we also investigated the probable signaling pathways involved in modulation of A2A R activation on CF expression in hypoxia-activated BV2 cells. Activation of A2A R promoted CF expression, which was significantly increased after the low glucose and hypoxia treatments in BV2 cells. CF gene knockdown markedly inhibited the increase in the expression of pro-inflammatory cytokines induced by A2A R activation in hypoxic-BV2 cells. Furthermore, the increased expression of the CF induced by A2A R activation was remarkably inhibited in hypoxic-BV2 cells administrated with the PKA inhibitor H-89 and the PKC inhibitor staurosporine. Hence, these results indicate that hypoxia BV2 cells highly express CF, which is involved in A2A R activation-mediated neuroinflammation via the PKA/CREB and PKC/CREB or ERK1/2 signaling pathways.
format	article
author	Wei Duan Haoxiang Wang Qinlin Fan Lin Chen Heqing Huang Hong Ran
author_facet	Wei Duan Haoxiang Wang Qinlin Fan Lin Chen Heqing Huang Hong Ran
author_sort	Wei Duan
title	Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
title_short	Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
title_full	Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
title_fullStr	Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
title_full_unstemmed	Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells
title_sort	cystatin f involvement in adenosine a2a receptor-mediated neuroinflammation in bv2 microglial cells
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/ae788e8298ef4a87975a562c4edcab2c
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Cystatin F involvement in adenosine A2A receptor-mediated neuroinflammation in BV2 microglial cells

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