A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model

• Main Authors: Jun Yu, Yan Yan, Yiye Chen, Yan Zheng, Xiaoyan Yu, Jialu Wang, Yafu Wang, Anken Wang, Xiaoli Kang, Jie Cen, Lingyan Dong, Li Li, Peiquan Zhao
• Format: Article
• Language: English
• Published: Hindawi Limited 2020-01-01
• Series: BioMed Research International
• Online Access: http://dx.doi.org/10.1155/2020/2054293

Background. The aim of this study was to research the effects of glutamine synthetase (GS) and glutamate aspartate transporter (GLAST) in rat Müller cells and the effects of an adenosine A2AR antagonist (SCH 442416) on GS and GLAST in hypoxia both in vivo and in vitro. Methods. This study used RT-PCR and Western blotting to quantify the expressions of GS and GLAST under different hypoxic conditions as well as the expressions of GS and GLAST at different drug concentrations. A cell viability assay was used to assess drug toxicity. Results. mRNA and protein expression of GS and GLAST in hypoxia Group 24 h was significantly increased. mRNA and protein expressions of GS and GLAST both increased in Group 1 μM SCH 442416 compared with other groups. One micromolar SCH 442416 could upregulate GS and GLAST’s activity in hypoxia both in vivo and in vitro. Conclusions. Hypoxia activates GS and GLAST in rat retinal Müller cells in a short time in vitro. (2) A2AR antagonists upregulate the activity of GS and GLAST in hypoxia both in vivo and in vitro.