impairment of hepcidin upregulation by lipopolysaccharide in the interleukin-6 knockout mouse brain

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2017
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Abstract
To find out whether the Interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in the expression of hepcidin in the mouse brain in vivo, we investigated the phosphorylation of STAT3, as well as the expression of hepcidin mRNA, ferroportin 1 (Fpn1) and ferritin light chain (Ft-L) proteins in the cortex and hippocampus of LPS-treated wild type (IL-6+/+) and IL-6 knockout (IL-6-/-) mice. We demonstrated that IL-6 knockout could significantly reduce the response of hepcidin mRNA, phospho-STAT3, Fpn1 and Ft-L protein expression to LPS treatment, in both the cortex and hippocampus of mice. Also, Stattic, an inhibitor of STAT3, significantly reduced the expression of phospho-STAT3 and hepcidin mRNA in the cortex and hippocampus of the LPS-treated wild type mice. These findings provide in vivo evidence for the involvement of the IL-6/STAT3 signaling pathway in the expression of hepcidin.
Reference Key
zhang2017frontiersimpairment Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Fa-Li Zhang, Hui-Min Hou, Zhi-Nan Yin, Lan Chang, Fe-Mi Li, Y.-J. Chen, Ya Ke, Zhong-Ming Qian
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Journal international journal of nanomedicine
Year 2017
DOI
10.3389/fnmol.2017.00367
URL
http://journal.frontiersin.org/article/10.3389/fnmol.2017.00367/full
Keywords
apoptosis isoniazid hepatotoxicity hepcidin mitochondrial biogenesis pharmacology neuropsychiatry biological psychiatry p38 mapktherapeutics

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