Transferrin stimulates iron absorption, exocytosis, and secretion in cultured intestinal cells

The cellular mechanism by which basolateral transferrin (Tf) produces an in crease in apical-to-basolateral Fe flux in Caco-2 cells was analyzed. After a pulse of Fe-59 from the apical medium, three types of basolateral Fe-59 efflux were found: a Fe-59 efflux that was independent of the presence of T f in the basolateral medium, a Fe-59 efflux in which Fe-59 left the cell bo und to Tf, and a Tf-dependent Fe-59 efflux in which Fe-59 came off the cell not bound to Tf. Furthermore, addition of Tf to the basolateral medium dou bled the exocytosis rate of Tf and increased the secretion of apolipoprotei n A, a basolateral secretion marker. Both apotransferrin and Fe-containing Tf produced similar increases in Fe-59 efflux, Tf exocytosis, and apolipopr otein A secretion. The Ca2+ channel inhibitor SKF-96365 inhibited both the Tf-mediated increase in transepithelial Fe transport and the secretion of a polipoprotein A. Thus the activation of transepithelial Fe transport by Tf seems to be mediated by Ca2+ entry into the cells.