Characterization of amino acid transport in human endothelial cells

• Published in: The American journal of physiology Vol. 265; no. 4 Pt 1; p. C1006
• Main Authors: Bussolati, O, Sala, R, Astorri, A, Rotoli, B M, Dall'Asta, V, Gazzola, G C
• Format: Journal Article
• Language: English
• Published: United States 01.10.1993
• Subjects: Amino Acids - metabolism; Anions - metabolism; Biological Transport; Cations - metabolism; Cells, Cultured; Endothelium, Vascular - cytology; Endothelium, Vascular - metabolism; Glutamine - metabolism; Humans; Intracellular Membranes - metabolism; Umbilical Veins - cytology; Umbilical Veins - metabolism
• ISSN: 0002-9513
• DOI: 10.1152/ajpcell.1993.265.4.c1006

The transport of amino acids has been studied in human umbilical vein endothelial cells. Neutral amino acids enter human umbilical vein endothelial cells through three distinct agencies endowed with the characteristics of systems A, ASC, and L. Each system has been studied by evaluating the influx of preferential substrates. The influx of L-proline and 2-methylaminoisobutyric acid occurs through an Na(+)-dependent adaptively regulated trans-inhibited agency identifiable with system A. L-Threonine influx occurs mainly through a distinct Na(+)-dependent trans-stimulated pathway corresponding to system ASC. System L accounts for Na(+)-independent influx of L-leucine. These systems cooperate for the transport of L-glutamine, which is due mainly to system ASC, whereas the component due to the operation of system A increases upon amino acid starvation. No clear evidence was found for a glutamine-specific system ("system N"). Two systems, one Na+ dependent (system XAG-) and the other Na+ independent (system xc-), transport anionic amino acids. L-Arginine influx exhibits a poor dependence on extracellular Na+, whereas it is sensitive to conditions known to change membrane potential and to trans-stimulation by intracellular amino acids. These features are consistent with a process mediated by system y+ and may be of significance for the regulation of the intracellular concentration of L-arginine.