The Effect of Drug Pre-treatment on Taurine Transport at the Inner Blood-Retinal Barrier Under Variable Conditions
Taurine is essential for the development and function of the central nervous system, retina, and cardiovascular system. It is a naturally occurring amino acid, abundantly found in the retina. It has been shown to exhibit antioxidant, neuroprotective, and osmoregulatory functions in the retina. We used conditionally immortalized rat retinal capillary endothelial cells (TR-iBRB), in vitro, to investigate the effects of oxidative stress, high glucose (HG) and hypertonic conditions on taurine transport. TR-iBRB cells pre-treated with tumor necrosis factor alpha (TNF-α) showed a significant increase in [3H]taurine uptake rate, which, however, decreased when treated with taurine (50 mM). Addition of paeonol and propranolol to TNF-α pre-treated cells had no significant effect on [3H]taurine uptake, but the addition of 10 mM taurine caused a reduction. The uptake rate decreased under HG conditions, in contrast to that under hypertonic conditions. [3H]Taurine uptake increased with pre-incubation time. Additionally, uptake of [3H]taurine and mRNA expression of taurine transporter (TauT) decreased significantly under hypertonic and HG conditions, following pre-incubation with 10 mM taurine, 1 mM paeonol, and 0.1 mM propranolol. [3H]Taurine uptake was significantly inhibited in the presence of taurine transporters such as taurine and β-alanine. Results indicate that oxidative stress and hypertonic conditions increased taurine uptake in iBRB cell lines, whereas HG conditions reduced the uptake rate. Taurine may be useful in stabilizing the microenvironment in cells affected by oxidative stress as well as hypertonic and HG conditions. Moreover, taurine may play a key role in maintaining taurine concentrations in the taurine transporter system of retinal cells.
KeywordsTaurine Inner blood-retinal barrier Hypertonic High glucose TNF-alpha Paeonol Propranolol
Inner blood retinal barrier
Real time polymerase chain reaction
tumor necrosis factor alpha
Our study was supported by a National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (No. 2011-0030074).
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