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

Abstract : 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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Blood, American Society of Hematology, 2016, [Epub ahead of print]. 〈10.1182/blood-2016-10-748541 〉
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http://www.hal.inserm.fr/inserm-01430303
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Dernière modification le : samedi 15 septembre 2018 - 01:08:44
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Céline Besson-Fournier, Aurélie Gineste, Chloé Latour, Ophélie Gourbeyre, Delphine Meynard, et al.. Hepcidin upregulation by inflammation is independent of Smad1/5/8 signaling by activin B Supplementary data. Blood, American Society of Hematology, 2016, [Epub ahead of print]. 〈10.1182/blood-2016-10-748541 〉. 〈inserm-01430303〉

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