THE EFFECT OF ERYTHROPOIETIN ON HEPCIDIN EXPRESSION IN HEPATIC CELLS INVOLVES PI3K/mTOR SIGNALING

SCHIAPPACASSE AGUSTINA; VITTORI DANIELA; MALTANERI ROMINA; NESSE ALCIRA; CHAMORRO MARÍA EUGENIA

Mar del Plata

Congreso; LXIII Reunión Científica de la Sociedad Argentina de Investigación Clinica; 2018

Sociedad Argentina de Investigación Clínica

Iron(Fe) homeostasis is essential for living organisms, since cells rely on thismicronutrient for a variety of metabolic processes. This is particularlyrelevant for stress erythropoiesis, when Fe stored in hepatocytes must bemobilized for its uptake by bone marrow erythroblasts and the subsequentsynthesis of hemoglobin. Hepatic stores are maintained by the peptide hepcidin(Hamp), which impairs Fe release by inducing degradation of the ferroportintransporter. In vivo,erythropoietin (Epo) has been shown to decrease Hamp levels, but questionsarise about this being a direct effect on hepatocytes, and about the possiblemechanisms involved.Inorder to study a possible direct action of Epo on Hamp production in hepaticcells, we assessed the ability of the cytokine to induce signaling in the humanhepatoblastoma cell line HepG2. EpoR receptor expression was detected in thiscell type (RT-PCR, flow cytometry). Epo (160 ng/mL) stimulated phosphorylationof the EpoR-associated kinase JAK2 (flow cytometry, Control: 20.9±3.1%, *Epo5?: 38.4±5.2%, *P