Anemia in beta-thalassemia patients targets hepatic hepcidin transcript levels independently of iron metabolism genes controlling hepcidin expression
Emilie Camberlein, Giuliana Zanninelli, Lénaïck Détivaud, Anna Rita Lizzi, Francesco Sorrentino, Stefania Vacquer, Marie-Bérengère Troadec, Emanuele Angelucci, Emmanuelle Abgueguen, Olivier Loréal, Paolo Cianciulli, Maria Eliana Lai, Pierre Brissot, Emilie Camberlein, Giuliana Zanninelli, Lénaïck Détivaud, Anna Rita Lizzi, Francesco Sorrentino, Stefania Vacquer, Marie-Bérengère Troadec, Emanuele Angelucci, Emmanuelle Abgueguen, Olivier Loréal, Paolo Cianciulli, Maria Eliana Lai, Pierre Brissot
Abstract
Thalassemia associates anemia and iron overload, two opposite stimuli regulating hepcidin gene expression. We characterized hepatic hepcidin expression in 10 thalassemia major and 13 thalassemia intermedia patients. Hepcidin mRNA levels were decreased in the thalassemia intermedia group which presented both lower hemoglobin and higher plasma soluble transferrin receptor levels. There was no relationship between hepcidin mRNA levels and those of genes controlling iron metabolism, including HFE, hemojuvelin, transferrin receptor-2 and ferroportin. These results underline the role of erythropoietic activity on hepcidin decrease in thalassemic patients and suggest that mRNA modulations of other studied genes do not have a significant impact.
Source: PubMed