HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/2/G301    most recent 00029.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Moriya, M. Articles by Linder, M. C. Search for Related Content PubMed PubMed Citation Articles by Moriya, M. Articles by Linder, M. C.

MUCOSAL BIOLOGY

Vesicular transport and apotransferrin in intestinal iron absorption, as shown in the Caco-2 cell model

Department of Chemistry and Biochemistry And Institute for Molecular Biology and Nutrition, California State University, Fullerton, California

Submitted 24 January 2005 ; accepted in final form 15 September 2005

The potential roles of vesicular transport and apotransferrin (entering from the blood) in intestinal Fe absorption were investigated using Caco-2 cell monolayers with tight junctions in bicameral chambers as a model. As shown previously, addition of 39 µM apotransferrin (apoTf) to the basolateral fluid during absorption studies markedly stimulated overall transport of 1 µM ⁵⁹Fe from the apical to the basal chamber and stimulated its basolateral release from prelabeled cells, implicating endo- and exocytosis. Rates of transport more than doubled. Uptake was also stimulated, but only 20%. Specific inhibitors of aspects of vesicular trafficking were applied to determine their potential effects on uptake, retention, and basolateral (overall) transport of ⁵⁹Fe. Nocodazole and 5'-(4-fluorosulfonylbenzoyl)-adenosine each reduced uptake and basolateral transport up to 50%. Brefeldin A inhibited about 10%. Tyrphostin A8 (AG10) reduced uptake 35% but markedly stimulated basolateral efflux, particularly that dependent on apoTf. Cooling of cells to 4°C (which causes depolymerization of microtubules and lowers energy availability) profoundly inhibited uptake and basolateral transfer of Fe (7- to 12-fold). Apical efflux (which was substantial) was not temperature affected. Our results support the involvement of apoTf cycling in intestinal Fe absorption and indicate that as much as half of the iron uses apoTf and non-apoTf-dependent vesicular pathways to cross the basolateral membrane and brush border of enterocytes.

endocytosis; exocytosis; polarized Caco-2 cell monolayers

This article has been cited by other articles:

				M. Shvartsman, R. Kikkeri, A. Shanzer, and Z. I. Cabantchik Non-transferrin-bound iron reaches mitochondria by a chelator-inaccessible mechanism: biological and clinical implications Am J Physiol Cell Physiol, October 1, 2007; 293(4): C1383 - C1394. [Abstract] [Full Text] [PDF]