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• W2172132512 endingPage "1296" @default.
• W2172132512 startingPage "1289" @default.
• W2172132512 abstract "Although system A is present at the blood-brain barrier (BBB), the physiological roles of system A have not been clarified. The efflux transport of the substrates of system A, such as L-proline (L-Pro), glycine (Gly), and alpha-methylaminoisobutyric acid (MeAIB), across the BBB was investigated using the in vivo Brain Efflux Index method. Over a period of 40 min, L-[(3)H]Pro and [(3)H]Gly underwent efflux from the brain, whereas [(3)H]MeAIB did not. The efflux of L-[(3)H]Pro was inhibited by the presence of unlabeled L-Pro and MeAIB, suggesting that carrier-mediated efflux transport of L-Pro across the BBB is involved in system A. L-[(3)H]Pro uptake by TR-BBB cells, used as an in vitro BBB model, was Na(+)-dependent with high-affinity (K(m1) = 425 microM) and low-affinity (K(m2) = 10.8 mM) saturable processes. The manner of inhibition of L-[(3)H]Pro uptake for amino acids was consistent with system A. Although GlnT, ATA2, and ATA3 mRNA were all expressed in TR-BBB cells, ATA2 mRNA was predominant. Under hypertonic conditions, ATA2 mRNA in TR-BBB cells was induced by up to 373%, and it activated [(3)H]MeAIB uptake. In light of these observations, our results indicate that L-Pro and Gly are transported from the brain across the BBB, whereas MeAIB is retained in the brain. System A is involved in efflux transport for L-Pro at the BBB. The predominantly expressed ATA2 mRNA at the BBB may play a role in maintaining the concentration of small neutral amino acids and cerebral osmotic pressure in the brain under pathological conditions." @default.
• W2172132512 created "2016-06-24" @default.
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• W2172132512 date "2002-06-01" @default.
• W2172132512 modified "2023-10-16" @default.
• W2172132512 title "ATA2 Is Predominantly Expressed as System A at the Blood-Brain Barrier and Acts as Brain-to-Blood Efflux Transport forl-Proline" @default.
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• W2172132512 doi "https://doi.org/10.1124/mol.61.6.1289" @default.
• W2172132512 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12021389" @default.
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