Effect of A2A receptor antagonist (SCH 442416) on the mRNA expression of glutamate aspartate transporter and glutamine synthetase in rat retinal Müller cells under hypoxic conditions in vitro

Yu,Jun; Huang,Xin; Wu,Qirong; Wang,Jun; Yu,Xiaoyan; Zhao,Peiquan

doi:10.3892/etm.2012.486

Effect of A2A receptor antagonist (SCH 442416) on the mRNA expression of glutamate aspartate transporter and glutamine synthetase in rat retinal Müller cells under hypoxic conditions in vitro

Authors:
- Jun Yu
- Xin Huang
- Qirong Wu
- Jun Wang
- Xiaoyan Yu
- Peiquan Zhao
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Affiliations: Department of Ophthalmology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China, Department of Ophthalmology, Eye and ENT Hospital, Shanghai Fudan University, Shanghai, P.R. China, Institute of Traumatology and Orthopaedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China, Department of Ophthalmology, The Fifth People's Hospital, Shanghai Fudan University, Shanghai, P.R. China
Published online on: February 13, 2012 https://doi.org/10.3892/etm.2012.486
Pages: 803-806

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Abstract

The purpose of the present study was to investigate the effect of the A2A receptor antagonist (SCH 442416) on the mRNA expression of glutamate aspartate transporter (GLAST) and glutamine synthetase (GS) in rat retinal Müller cells under hypoxic conditions in vitro. Immunofluorescent staining of GS and GFAP was used for the identification of Müller cells. The GLAST and GS mRNA expression of Müller cells treated with 0.1, 1 and 10 µM SCH 442416 under hypoxic conditions was examined by real-time PCR. Müller cells increased the mRNA expression of GLAST under hypoxic conditions; those treated with 0.1 µM SCH 442416 showed a further significant increase in the mRNA expression of GLAST in vitro. Although the mRNA expression of GS was decreased under hypoxic conditions, the mRNA expression was increased when Müller cells were treated with 0.1 µM SCH 442416. A2A receptor antagonist increased the GLAST and GS expression of Müller cells and accelerated the clearance of extracellular glutamate under hypoxic conditions in vitro.

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