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Hepcidin upregulation by inflammation is independent of Smad1/5/8 signaling by activin B Supplementary data

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Besson-Fournier, Céline | Gineste, Aurélie | Latour, Chloé | Gourbeyre, Ophélie | Meynard, Delphine | Martin, Patricia | Oswald, Eric | Coppin, Hélène | Roth, Marie-Paule

Edité par CCSD ; American Society of Hematology -

International audience. Activin B, which is strongly induced by inflammatory stimuli in the mouse liver, has recently appeared as a potent inductor of hepcidin in vitro, via the crossactivation of non-canonical SMAD1/5/8 signaling1,2. To confirm the cause and effect relationship between activin B, Smad1/5/8 phosphorylation, and hepcidin in vivo, we challenged Inhbb-/- mice (deficient in activin B) with LPS or infected them with a E. coli septicemic strain. Our data show that full induction of hepcidin expression by inflammatory stimuli requires a functional BMP6-activated signaling pathway in the hepatocyte but is independent of activin B and its activation of Smad1/5/8 signaling that likely occurs in other cells of the liver.

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