Abstract
We found that tumor necrosis factor α (TNFα)-induced apoptosis in HeLa cells was accompanied by a ∼2-fold increase in H- and L-ferritin and a decrease in transferrin receptor, two indices of increased iron availability. Iron supplementation and overexpression of H-ferritin or its mutant with an inactivated ferroxidase center reduced by about ∼50% the number of apoptotic cells after TNFα-treatment, while overexpression of L-ferritin was ineffective. The data indicate that H-ferritin has an anti-apoptotic activity unrelated to its ferroxidase activity and to its capacity to modify cellular iron metabolism.
Original language | English |
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Pages (from-to) | 187-192 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 537 |
Issue number | 1-3 |
DOIs | |
Publication status | Published - Feb 27 2003 |
Keywords
- Ferritin
- Iron metabolism
- Iron regulatory protein
- Oxidative damage
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology