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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2377-2383. Prepublished online as a Blood First Edition Paper on November 13, 2003; DOI 10.1182/blood-2003-06-1842. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-06-1842v1 103/6/2377    most recent 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 PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cozzi, A. Articles by Arosio, P. Search for Related Content PubMed PubMed Citation Articles by Cozzi, A. Articles by Arosio, P. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Analysis of the biologic functions of H- and L-ferritins in HeLa cells by transfection with siRNAs and cDNAs: evidence for a proliferative role of L-ferritin Anna Cozzi, Barbara Corsi, Sonia Levi, Paolo Santambrogio, Giorgio Biasiotto, and Paolo Arosio From Department of Biological and Technological Research, Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS), San Raffaele, Milano, Italy; Department M.T. and Biomedical Technologies, University of Brescia, Italy. We describe the use of small interfering RNAs (siRNAs) to down-regulate H- and L-ferritin levels in HeLa cells. siRNAs repressed H- and L-ferritin expression to about 20% to 25% of the background level in both stable and transient transfections. HeLa cells transfected with H- and L-ferritin cDNAs were analyzed in parallel to compare the effects of ferritin up- and down-regulation. We found that large modifications of L-ferritin levels did not affect iron availability in HeLa cells but positively affected cell proliferation rate in an iron-independent manner. The transient down-regulation of H-ferritin modified cellular iron availability and resistance to oxidative damage, as expected. In contrast, the stable suppression of H-ferritin in HeLa cell clones transfected with siRNAs did not increase cellular iron availability but made cells less resistant to iron supplementation and chelation. The results indicate that L-ferritin has no direct effects on cellular iron homeostasis in HeLa cells, while it has new, iron-unrelated functions. In addition, they suggest that H-ferritin function is to act as an iron buffer. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. C. Sammarco, S. Ditch, A. Banerjee, and E. Grabczyk Ferritin L and H Subunits Are Differentially Regulated on a Post-transcriptional Level J. Biol. Chem., February 22, 2008; 283(8): 4578 - 4587. [Abstract] [Full Text] [PDF] W. Wang, X. Di, R. B. D'Agostino Jr., S. V. Torti, and F. M. Torti Excess Capacity of the Iron Regulatory Protein System J. Biol. Chem., August 24, 2007; 282(34): 24650 - 24659. [Abstract] [Full Text] [PDF] P. Robach, G. Cairo, C. Gelfi, F. Bernuzzi, H. Pilegaard, A. Vigano, P. Santambrogio, P. Cerretelli, J. A. L. Calbet, S. Moutereau, et al. Strong iron demand during hypoxia-induced erythropoiesis is associated with down-regulation of iron-related proteins and myoglobin in human skeletal muscle Blood, June 1, 2007; 109(11): 4724 - 4731. [Abstract] [Full Text] [PDF] P. Cavadini, G. Biasiotto, M. Poli, S. Levi, R. Verardi, I. Zanella, M. Derosas, R. Ingrassia, M. Corrado, and P. 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