A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model. (28th October 2020)

• Record Type: Journal Article
• Authors: Yu, Jun; Yan, Yan; Chen, Yiye; Zheng, Yan; Yu, Xiaoyan; Wang, Jialu; Wang, Yafu; Wang, Anken; Kang, Xiaoli; Cen, Jie; Dong, Lingyan; Li, Li; Zhao, Peiquan
• Other Names: Cao Xin Guest Editor.
• Is Part Of: BioMed research international. Volume 2020(2020)
• Publication Date: 2020-10-28
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2020/2054293
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : 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 A2A R 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 μ M 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) A2A R antagonists upregulate the activity of GS and GLAST in hypoxia both in vivo and in vitro .