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High Glucose-Induced TRPC6 Channel Activation Decreases Glutamate Uptake in Rat Retinal MÃ1⁄4ller Cells by Ma, Mingming; Zhao, Shuzhi; Zhang, Jian; Sun, Tao; Fan, Ying; Zheng, Zhi is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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High glucose (HG) increases the production of reactive oxygen species (ROS), leading to decreased glutamate uptake in Müller cells. The transient receptor potential cation channel 6 (TRPC6) channel, an oxidative stress-sensitive Ca^2+^-permeable cationic channel, is readily detected in Müller cells and highly expressed under HG conditions. Yet, the effect of high glucose-induced TRPC6 channel activation in Müller cells is poorly understood. We hypothesized that TRPC6 channel activation mediates high glucose-induced decreases in Müller cell glutamate uptake. We found RNA interference (RNAi) of the TRPC6 channel abolished HG-induced decreases in glutamate uptake and cell death. HG also decreased the expression of the glutamate-aspartate transporter (GLAST), which is the most important transporter involved in glutamate uptake. The mRNA level of ciliary neurotrophic factor (CNTF) in rMC-1 cells and the release of CNTF in the culture media was decreased, but the mRNA levels of IL-6 and vascular endothelial growth factor (VEGF) were increased under HG conditions. After RNAi silencing in rMC-1 cells, the mRNA levels of CNTF increased, but IL-6 and VEGF levels decreased. Furthermore, TRPC6

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Author

Ma, Mingming; Zhao, Shuzhi; Zhang, Jian; Sun, Tao; Fan, Ying; Zheng, Zhi

Publisher

Frontiers; Frontiers Media SA; Frontiers Media S.A.; Lausanne: Frontiers Media S.A., 2010- (ISSN 1663-9812)

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)