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A(2A)R Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model

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 A(2A)R antagonist (SCH 442416) on GS and GLAST in hypoxia both in vivo and in vitro. METHODS: This study used RT-...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641686/
https://www.ncbi.nlm.nih.gov/pubmed/33195689
http://dx.doi.org/10.1155/2020/2054293
Descripción
Sumario: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 A(2A)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 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) A(2A)R antagonists upregulate the activity of GS and GLAST in hypoxia both in vivo and in vitro.