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Liver HFE protein content is posttranscriptionally decreased in iron-deficient mice and rats
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SYSNO ASEP 0503582 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Liver HFE protein content is posttranscriptionally decreased in iron-deficient mice and rats Author(s) Frýdlová, J. (CZ)
Rogalsky, D.W. (CZ)
Truksa, Jaroslav (BTO-N) RID, ORCID
Traeger, L. (CZ)
Steinbicker, A. U. (DE)
Vokurka, M. (DE)
Krijt, J. (CZ)Number of authors 7 Source Title American Journal of Physiology-Gastrointestinal and Liver Physiology. - : American Physiological Society - ISSN 0193-1857
Roč. 315, č. 4 (2018), G560-G568Number of pages 9 s. Language eng - English Country US - United States Keywords ALK3 ; hemojuvelin ; hepcidin ; matriptase-2 Subject RIV EB - Genetics ; Molecular Biology OECD category Gastroenterology and hepatology R&D Projects GA13-28830S GA ČR - Czech Science Foundation (CSF) Institutional support BTO-N - RVO:86652036 UT WOS 000447163500013 EID SCOPUS 85054081900 DOI 10.1152/ajpgi.00070.2018 Annotation Although the relationship between hereditary hemochromatosis and mutations in the HFE gene was discovered more than 20 years ago, information on the in vivo regulation of HFE protein expression is still limited. The purpose of the study was to determine the response of liver HFE protein content to iron deficiency in mice and rats by immunoblotting. Attempts to visualize the HFE protein in whole liver homogenates were unsuccessful, however, HFE could be detected in liver microsomes or in plasma membrane-enriched fractions. Five-week-old male C57BL/6 mice fed an iron-deficient diet for 4 wk presented with a significant decrease in liver iron content and liver Hamp expression, as well as with a significant decrease in liver HFE protein content. Rats fed an iron-deficient diet for 4 wk also displayed significant decrease in liver Hamp expression and liver HFE protein content. These results suggest that the downregulation of HFE-dependent signaling may contribute to decreased Hamp gene expression in states of prolonged iron deficiency. It has recently been proposed that HFE protein could be a potential target of matriptase-2, a hepatocyte protease mutated in iron-refractory iron deficiency anemia. However, immunoblot analysis of HFE protein in the livers from Tmprss6-mutated mask mice did not show evidence of matriptase-2-dependent HFE protein cleavage. In addition, no indication of HFE protein cleavage was seen in iron-deficient rats, whereas the full-length matriptase-2 protein content in the same animals was significantly increased. These results suggest that HFE is probably not a major physiological target of matriptase-2. Workplace Institute of Biotechnology Contact Monika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700 Year of Publishing 2019
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