2. Academic Validation
  3. A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model

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

  • Biomed Res Int. 2020 Oct 26;2020:2054293. doi: 10.1155/2020/2054293.
Jun Yu 1,  Yan Yan 2 3,  Yiye Chen 1,  Yan Zheng 1,  Xiaoyan Yu 4,  Jialu Wang 1,  Yafu Wang 1,  Anken Wang 1,  Xiaoli Kang 1,  Jie Cen 1,  Lingyan Dong 1,  Li Li 5,  Peiquan Zhao 1
Affiliations

Affiliations

  • 1 Department of Ophthalmology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China.
  • 2 Department of Ophthalmology, Stanford University School of Medicine, Stanford, California 94303, USA.
  • 3 Department of Ophthalmology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.
  • 4 Department of Ophthalmology, The Fifth People's Hospital of Shanghai, Shanghai 200240, China.
  • 5 Department of Ophthalmology, Shanghai Tenth People's Hospital, Affiliated Tongji University, Shanghai 200072, China.
PMID: 33195689 DOI: 10.1155/2020/2054293
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.

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