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The l-isomer-selective transport of aspartic acid is mediated by ASCT2 at the blood-brain barrier.

Authors: Tetsuka, Kazuhiro  Takanaga, Hitomi  Ohtsuki, Sumio  Hosoya, Ken-ichi  Terasaki, Tetsuya 
Citation: Tetsuka K, etal., J Neurochem. 2003 Nov;87(4):891-901. doi: 10.1046/j.1471-4159.2003.02063.x.
Pubmed: (View Article at PubMed) PMID:14622120
DOI: Full-text: DOI:10.1046/j.1471-4159.2003.02063.x

Aspartic acid (Asp) undergoes l-isomer-selective efflux transport across the blood-brain barrier (BBB). This transport system appears to play an important role in regulating l- and d-Asp levels in the brain. The purpose of this study was to identify the responsible transporters and elucidate the mechanism for l-isomer-selective Asp transport at the BBB. The l-isomer-selective uptake of Asp by conditionally immortalized mouse brain capillary endothelial cells used as an in vitro model of the BBB took place in an Na+- and pH-dependent manner. This process was inhibited by system ASC substrates such as l-alanine and l-serine, suggesting that system ASC transporters, ASCT1 and ASCT2, are involved in the l-isomer selective transport. Indeed, l-Asp uptake by oocytes injected with either ASCT1 or ASCT2 cRNA took place in a similar manner to that in cultured BBB cells, whereas no significant d-Asp uptake occurred. Although both ASCT1 and ASCT2 mRNA were expressed in the cultured BBB cells, the expression of ASCT2 mRNA was 6.7-fold greater than that of ASCT1. Moreover, immunohistochemical analysis suggests that ASCT2 is localized at the abluminal side of the mouse BBB. These results suggest that ASCT2 plays a key role in l-isomer-selective Asp efflux transport at the BBB.


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CRRD Object Information
CRRD ID: 21201277
Created: 2020-02-29
Species: All species
Last Modified: 2020-02-29
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.