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Iron‐induced oxidative stress up‐regulates calreticulin levels in intestinal epithelial (Caco‐2) cells
Author(s) -
Núñez Marco T.,
Osorio Andrea,
Tapia Victoria,
Vergara Alexander,
Mura Casilda V.
Publication year - 2001
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.1194
Subject(s) - calreticulin , endoplasmic reticulum , oxidative stress , chaperone (clinical) , microbiology and biotechnology , ferritin , caco 2 , ferroportin , cytosol , oxidative phosphorylation , heat shock protein , hepcidin , chemistry , microsome , protein disulfide isomerase , hsp70 , biology , biochemistry , metabolism , immunology , in vitro , medicine , inflammation , enzyme , pathology , gene , iron homeostasis
Calreticulin, a molecular chaperone involved in the folding of endoplasmic reticulum synthesized proteins, is also a shock protein induced by heat, food deprivation, and chemical stress. Mobilferrin, a cytosolic isoform of calreticulin, has been proposed to be an iron carrier for iron recently incoming into intestinal cells. To test the hypothesis that iron could affect calreticulin expression, we investigated the possible associations of calreticulin with iron metabolism. To that end, using Caco‐2 cells as a model of intestinal epithelium, the mass and mRNA levels of calreticulin were evaluated as a function of the iron concentration in the culture media. Increasing the iron content in the culture from 1 to 20 μM produced an increase in calreticulin mRNA and a two‐fold increase in calreticulin. Increasing iron also induced oxidative damage to proteins, as assessed by the formation of 4‐hydroxy‐2‐nonenal adducts. Co‐culture of cells with the antioxidants quercetin, dimethyltiourea and N‐acetyl cysteine abolished both the iron‐induced oxidative damage and the iron‐induced increase in calreticulin. We postulate that the iron‐induced expression of calreticulin is part of the cellular response to oxidative stress generated by iron. J. Cell. Biochem. 82: 660–665, 2001. © 2001 Wiley‐Liss, Inc.