1. A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model
- Author
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Yi-ye Chen, Xiaoli Kang, Peiquan Zhao, Ling-yan Dong, Anken Wang, Jia-Lu Wang, Yafu Wang, Yan Yan, Li Li, Jun Yu, Xiaoyan Yu, Yan Zheng, and Jie Cen
- Subjects
Article Subject ,General Immunology and Microbiology ,biology ,Chemistry ,General Medicine ,Hypoxia (medical) ,Adenosine ,Molecular biology ,General Biochemistry, Genetics and Molecular Biology ,In vitro ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,In vivo ,Glutamine synthetase ,030221 ophthalmology & optometry ,medicine ,Glutamate aspartate transporter ,biology.protein ,Medicine ,Viability assay ,medicine.symptom ,030217 neurology & neurosurgery ,medicine.drug - 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 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.
- Published
- 2020
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