Blog
About

5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Erythropoietin administration increases splenic erythroferrone protein content and liver TMPRSS6 protein content in rats.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Erythroferrone (ERFE) and TMPRSS6 are important proteins in the regulation of iron metabolism. The objective of the study was to examine splenic ERFE and liver TMPRSS6 synthesis in rats treated with a combination of iron and erythropoietin (EPO). EPO was administered to female Wistar rats at 600U/day for four days, iron-pretreated rats received 150mg of iron before EPO treatment. Content of ERFE and TMPRSS6 proteins was determined by commercial antibodies. Iron pretreatment prevented the EPO-induced decrease in hepcidin expression. Content of phosphorylated SMAD 1,5,8 proteins was decreased in the liver by both EPO and iron plus EPO treatment. Fam132b expression in the spleen was increased both by EPO and iron plus EPO treatments; these treatments also significantly induced splenic Fam132a expression. ERFE protein content in the spleen was increased both by EPO and iron plus EPO to a similar extent. EPO administration increased TMPRSS6 content in the plasma membrane-enriched fraction of liver homogenate; in iron-pretreated rats, this increase was abolished. The results confirm that iron pretreatment prevents the EPO-induced decrease in liver Hamp expression. This effect probably occurs despite high circulating ERFE levels, since EPO-induced ERFE protein synthesis is not influenced by iron pretreatment.

          Related collections

          Author and article information

          Journal
          Blood Cells Mol. Dis.
          Blood cells, molecules & diseases
          Elsevier BV
          1096-0961
          1079-9796
          May 2017
          : 64
          Affiliations
          [1 ] Institute of Pathological Physiology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
          [2 ] Institute of Biotechnology, BIOCEV Research Center, Czech Academy of Sciences, Prague, Czech Republic.
          [3 ] Institute of Pathological Physiology, First Faculty of Medicine, Charles University, Prague, Czech Republic. Electronic address: jkri@lf1.cuni.cz.
          Article
          S1079-9796(17)30078-5
          10.1016/j.bcmd.2017.02.007
          28282554

          Fam132a, Fam132b, Hemojuvelin, Hepcidin, TMPRSS6

          Comments

          Comment on this article