Liver HFE protein content is posttranscriptionally decreased in iron-deficient mice and rats

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10381973" target="_blank" >RIV/00216208:11110/18:10381973 - isvavai.cz</a>

Alternative codes found

RIV/86652036:_____/18:00503582

Result on the web

<a href="https://doi.org/10.1152/ajpgi.00070.2018" target="_blank" >https://doi.org/10.1152/ajpgi.00070.2018</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1152/ajpgi.00070.2018" target="_blank" >10.1152/ajpgi.00070.2018</a>

Result language

angličtina

Original language name

Liver HFE protein content is posttranscriptionally decreased in iron-deficient mice and rats

Original language description

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. NEW &amp; NOTEWORTHY Feeding of iron-deficient diet for 4 wk decreased liver HFE protein content in both mice and rats, suggesting that decreased HFE-dependent signaling may contribute to hepcidin downregulation in iron deficiency. There was no difference in HFE protein band appearance between matriptase-2-mutated mask mice and wild-type mice, indicating that HFE is probably not a major physiological substrate of matriptase-2-mediated protease activity in vivo.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30105 - Physiology (including cytology)

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

American Journal of Physiology - Gastrointestinal and Liver Physiology

ISSN

0193-1857

e-ISSN

—

Volume of the periodical

315

Issue of the periodical within the volume

4

Country of publishing house

US - UNITED STATES

Number of pages

9

Pages from-to

"G560"-"G568"

UT code for WoS article

000447163500013

EID of the result in the Scopus database

2-s2.0-85054081900