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

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posted on 2024-07-16, 05:46 authored by Wei DuanWei Duan, Haoxiang Wang, Qinlin Fan, Lin Chen, Heqing Huang, Hong Ran
AbstractOur 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.

History

Journal

Scientific Reports

Volume

8

Article number

6820

Pagination

1-14

Location

London, Eng.

Open access

  • Yes

ISSN

2045-2322

eISSN

2045-2322

Language

en

Publication classification

C1.1 Refereed article in a scholarly journal

Issue

1

Publisher

Nature Portfolio