Regulation of taurine transport at the blood–brain barrier by tumor necrosis factor‐α, taurine and hypertonicity
Taurine is the abundant sulfur‐containing β‐amino acid in brain where it exerts a neuroprotective effect. Although it is known that the blood–brain barrier (BBB) mediates taurine transport, the regulation of taurine transport have not been clarified yet. A conditionally immortalized rat brain capill...
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Published in: | Journal of neurochemistry Vol. 83; no. 5; pp. 1188 - 1195 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Oxford, UK
Blackwell Science Ltd
01-12-2002
Blackwell |
Subjects: | |
Online Access: | Get full text |
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Summary: | Taurine is the abundant sulfur‐containing β‐amino acid in brain where it exerts a neuroprotective effect. Although it is known that the blood–brain barrier (BBB) mediates taurine transport, the regulation of taurine transport have not been clarified yet. A conditionally immortalized rat brain capillary endothelial cells (TR‐BBB13), an in vitro model of the BBB, exhibited [3H]taurine uptake, which was dependent on both Na+ and Cl–, and inhibited by β‐alanine. Taurine transporter (TAUT) mRNA was detected in TR‐BBB13 cells, and TAUT protein was also expressed at 70 kDa. TR‐BBB13 cells exposed to 20 ng/mL TNF‐α and under hypertonic conditions showed a 1.7‐fold and 3.2‐fold increase in [3H]taurine uptake, respectively. In contrast, lipopolysaccharide and diethyl maleate did not significantly affect taurine uptake. The taurine uptake was reduced by pre‐treatment with excess taurine (50 mm). The mRNA level of the TAUT in TNF‐α and following hypertonic treatment was greater than that in control cells, whereas that under excess taurine conditions was lower than in controls. Therefore, taurine transport activity at the BBB appears to be regulated at the transcriptional level by cell damage, osmolality and taurine in the brain. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-3042 1471-4159 |
DOI: | 10.1046/j.1471-4159.2002.01223.x |