Amino acid transport in podocytes

It has recently been shown that formation of podocyte foot processes is dep endent on a constant source of lipids and proteins (Simons M, Saffrich R, R eiser J, and Mundel P. J Am Soc Nephrol 10: 1633-1639, 1999). Here we chara cterize amino acid transport mechanisms in differentiated cultured podocyte s and investigate whether it may be disturbed during podocyte injury. RT-PC R studies detected mRNA for transporters of neutral amino acids (ASCT1, ASC T2, 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), ser ine (Ser), threonine (Thr), glutamic acid (Glu), arginine (Arg), and histid ine (His) depolarized podocytes and increased their whole cell conductances . Depletion of extracellular Na+ completely inhibited the depolarization in duced 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 mu g/ml puromycin aminonucleos ide for 24 h significantly attenuated the effects induced by the various am ino acids by similar to 70%. The data indicate the existence of different a mino acid transporter systems in podocytes. Alteration of amino acid transp ort may participate in podocyte injury and disturbed foot process formation .