Abstract：
:Hepcidin (Hepc) is a 25 amino acid cationic peptide with broad antibacterial and antifungal actions. A likely role for Hepc in iron metabolism was suggested by the observation that mice having disruption of the gene encoding the transcription factor USF2 failed to produce Hepc mRNA and developed spontaneous visceral iron overload. Lately, Hepc has been considered the "stores regulator," a putative factor that signals the iron content of the body to intestinal cells. In this work, we characterized the effect of Hepc produced by hepatoma cells on iron absorption by intestinal cells. To that end, human Hepc cDNA was cloned and overexpressed in HepG2 cells and conditioned media from Hepc-overexpressing cells was used to study the effects of Hepe on intestinal Caco-2 cells grown in bicameral inserts. The results indicate that Hepc released by HepG2 inhibited apical iron uptake by Caco-2 cells, probably by inhibiting the expression of the apical transporter DMT1. These results support a model in which Hepc released by the liver negatively regulates the expression of transporter DMT1 in the enterocyte.
journal_name
Biol Resjournal_title
Biological researchauthors
Mena NP,Esparza AL,Núñez MTdoi
10.4067/s0716-97602006000100022subject
Has Abstractpub_date
2006-01-01 00:00:00pages
191-3issue
1eissn
0716-9760issn
0717-6287pii
S0716-97602006000100022journal_volume
39pub_type
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更新日期：1997-01-01 00:00:00
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更新日期：1998-01-01 00:00:00
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更新日期：1993-01-01 00:00:00
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doi：10.4067/s0716-97602006000100012
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