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Am J Physiol Renal Physiol 278: F999-F1005, 2000;
0363-6127/00 $5.00
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Vol. 278, Issue 6, F999-F1005, June 2000

Amino acid transport in podocytes

Joachim Gloy1, Steffen Reitinger1, Karl-Georg Fischer1, Rainer Schreiber2, Anissa Boucherot2, Karl Kunzelmann2, Peter Mundel3, and Hermann Pavenstädt1

1 Department of Medicine, Division of Nephrology, and 2 Department of Physiology, Albert-Ludwigs-University Freiburg, D-79106 Freiburg, Germany; and 3 Department of Medicine and Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York

It has recently been shown that formation of podocyte foot processes is dependent on a constant source of lipids and proteins (Simons M, Saffrich R, Reiser J, and Mundel P. J Am Soc Nephrol 10: 1633-1639, 1999). Here we characterize amino acid transport mechanisms in differentiated cultured podocytes and investigate whether it may be disturbed during podocyte injury. RT-PCR studies detected mRNA for transporters of neutral amino acids (ASCT1, ASCT2, and B0/+), cationic AA (CAT1 and CAT3), and anionic AA (EAAT2 and EAAT3). Alanine (Ala), asparagine, cysteine (Cys), glutamine (Gln), glycine (Gly), leucine (Leu), methionine (Met), phenylalanine (Phe), proline (Pro), serine (Ser), threonine (Thr), glutamic acid (Glu), arginine (Arg), and histidine (His) depolarized podocytes and increased their whole cell conductances. Depletion of extracellular Na+ completely inhibited the depolarization induced by Ala, Gln, Glu, Gly, Leu, and Pro and decreased the depolarization induced by Arg and His, indicating the presence of Na+-dependent amino acid transport. Incubation of podocytes with 100 µg/ml puromycin aminonucleoside for 24 h significantly attenuated the effects induced by the various amino acids by ~70%. The data indicate the existence of different amino acid transporter systems in podocytes. Alteration of amino acid transport may participate in podocyte injury and disturbed foot process formation.

podocytes; amino acid transport; puromycin


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