Skip to Main content Skip to Navigation
Journal articles

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.
Document type :
Journal articles
Complete list of metadatas

https://www.hal.inserm.fr/inserm-01430303
Contributor : Marie-Paule Roth <>
Submitted on : Monday, January 9, 2017 - 4:40:39 PM
Last modification on : Tuesday, May 26, 2020 - 8:45:54 PM
Long-term archiving on: : Monday, April 10, 2017 - 4:15:36 PM

Files

letter actB KO.pdf
Files produced by the author(s)

Identifiers

Collections

Citation

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, 129 (4), [Epub ahead of print]. ⟨10.1182/blood-2016-10-748541⟩. ⟨inserm-01430303⟩

Share

Metrics

Record views

197

Files downloads

338