| First Author | Picard V | Year | 1998 |
| Journal | J Biol Chem | Volume | 273 |
| Issue | 25 | Pages | 15382-6 |
| PubMed ID | 9624120 | Mgi Jnum | J:49408 |
| Mgi Id | MGI:1277453 | Doi | 10.1074/jbc.273.25.15382 |
| Citation | Picard V, et al. (1998) Role of ferritin in the control of the labile iron pool in murine erythroleukemia cells. J Biol Chem 273(25):15382-6 |
| abstractText | In vitro studies have shown that ferritin iron incorporation is mediated by a ferroxidase activity associated with ferritin H subunits (H-Ft) and a nucleation center associated with ferritin L subunits (L-Ft). To assess the role played by the ferritin subunits in regulating intracellular iron distribution, we transfected mouse erythroleukemia cells with the H-Ft subunit gene mutated in the iron-responsive element. Stable transfectants displayed high H-Ft levels and reduced endogenous L-Ft levels, resulting in a marked change in the H:L subunit ratio from 1:1 in control cells to as high as 20:1 in some transfected clones. The effects of H-Ft overexpression on the labile iron pool were determined in intact cells by a novel method based on the fluorescent metallosensor calcein. H-Ft overexpression resulted in a significant reduction in the iron pool, from 1.3 microM in control cells to 0.56 microM in H-Ft transfectants, and in higher buffering capacity following iron loads. A fraction of the H-Ft-associated iron was labile, available to cell-permeant, but not cell-impermeant, chelators. The results of this study provide the first in vivo direct demonstration of the capacity of H-Ft to sequester cell iron and to regulate the levels of the labile iron pool. |
