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

Jun Yu1, Yan Yan2,3, Yiye Chen1

  • 1Department of Ophthalmology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China.

Biomed Research International
|November 16, 2020
PubMed
Abstract

Insights

Hypoxia increases glutamine synthetase (GS) and glutamate aspartate transporter (GLAST) in rat Müller cells. Adenosine A2A receptor antagonists further upregulate GS and GLAST activity under hypoxic conditions.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Ophthalmology

Background:

  • Investigates glutamine synthetase (GS) and glutamate aspartate transporter (GLAST) in rat Müller cells.
  • Examines the impact of adenosine A2A receptor (A2AR) antagonist SCH 442416 on GS and GLAST.
  • Studies effects under both in vivo and in vitro hypoxic conditions.

Purpose of the Study:

  • To determine the role of GS and GLAST in rat Müller cells during hypoxia.
  • To evaluate the effect of the A2AR antagonist SCH 442416 on GS and GLAST expression and activity.

Main Methods:

  • Quantitative analysis of GS and GLAST expression using RT-PCR and Western blotting.
  • Assessment of drug toxicity via cell viability assays.
  • Evaluation under varying hypoxic conditions and drug concentrations.

Main Results:

  • Hypoxia significantly increased both mRNA and protein expression of GS and GLAST.
  • 1 µM SCH 442416 demonstrated a notable increase in GS and GLAST expression compared to other groups.
  • The A2AR antagonist SCH 442416 upregulated GS and GLAST activity in hypoxic conditions.

Conclusions:

  • Hypoxia rapidly activates GS and GLAST in rat retinal Müller cells.
  • A2AR antagonists enhance the activity of GS and GLAST under hypoxic conditions, both in vivo and in vitro.

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