Effect of erythropoietin in bronchial cells in an iron excess mouse model

Abstract

Imbalances of iron homeostasis are implicated in acute and chronic lung diseases. However, the mechanisms involved in pulmonary iron deposition and its role in the pathogenesis of lung diseases remains unknown. The aim was evaluate the effect of erythropoietin on bronquial cells in an iron excess mouse model studying the regulatory proteins of the iron cycle CF1 mice(25±5g; 3 months-old) were divided into 4 groups(n=4/group):1)Control; 2)Iron-overload(iron saccharate;days0,4,8,12 ip;1800mg/kg); 3)EPO(days17,18,19) ip;20000UI/kg);4)Iron-overload+EPO. Immunohistochemistry: anti-prohepcidin, L-ferritin, DMT1(divalent metal transporter1) and ZIP14(Zrt-Irt-like Protein14) followed by Perl´s staining. The Protocol was approved by the CICUAE; UNS.We observe that the DMT1 localization in bronchial cells was cytoplasmatic in iron overload+EPO, control and EPO whille in overload the importer was in the apical zone and in membrane cells.ZIP14 expression in bronchial cells was evident in iron overload while it was slight iron overload+EPO, control and EPO.In control and EPO hemosiderin was absent while in Iron overload and iron overload+EPO it was abundant in alveoli.The L-ferritin expression in iron overload was intense in alveoli and apical in bronchial cells. However it expression in iron overload+EPO was cytoplasmic in bronchial cells. It expression was slight in alveoli and cytoplasmatic in bronchial cells of control and EPO.The prohepcidin expression was similar in all conditions.The decrease of ZIP14 expression, and the change in the DMT1 and L-ferritin localization in Iron overload+EPO compared to iron overload, could be reflecting a lower iron uptake and storage in bronchial cells in EPO presence, suggesting a protective mechanism EPO-DEPENDENT.