HIF-mediated increased ROS from reduced mitophagy and decreased catalase causes neocytolysis

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F15%3A33157096" target="_blank" >RIV/61989592:15110/15:33157096 - isvavai.cz</a>

Result on the web

<a href="http://link.springer.com/article/10.1007/s00109-015-1294-y/fulltext.html" target="_blank" >http://link.springer.com/article/10.1007/s00109-015-1294-y/fulltext.html</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00109-015-1294-y" target="_blank" >10.1007/s00109-015-1294-y</a>

Result language

angličtina

Original language name

HIF-mediated increased ROS from reduced mitophagy and decreased catalase causes neocytolysis

Original language description

During prolonged hypoxia, hypoxia-inducible factors (HIFs) mediate an increase in erythropoiesis, leading to an increased red blood cell (RBC) mass and polycythemia. Upon return to normoxia, the increased RBC mass is abruptly overcorrected by the preferential destruction of hypoxia-formed young RBCs, a phenomenon termed neocytolysis. We developed a murine model of neocytolysis by exposing mice to 12 % oxygen for 10 days followed by return to normoxia. Upon return to normoxia, there was excessive accumulation of reactive oxygen species (ROS) in RBCs from an increased reticulocyte mitochondrial mass correlating with decreased Bnip3L transcripts (Bnip3L mediates reticulocyte mitophagy) and reduced catalase activity. During hypoxia, upregulated miR-21 resulted in low catalase activity in young RBCs. Together, these experiments indicate that the major mechanisms causing neocytolysis involve (1) production of young RBCs with low catalase during hypoxia and (2) lysis of the young RBCs after r

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

ED - Physiology

OECD FORD branch

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Project

<a href="/en/project/GA15-13732S" target="_blank" >GA15-13732S: Molecular basis of erythroid defect and disrupted iron metabolism in DMT1 deficiency and Diamond-Blackfan anemia</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2015

Confidentiality

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

Name of the periodical

Journal of Molecular Medicine

ISSN

0946-2716

e-ISSN

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Volume of the periodical

93

Issue of the periodical within the volume

8

Country of publishing house

DE - GERMANY

Number of pages

10

Pages from-to

857-866

UT code for WoS article

000358326500005

EID of the result in the Scopus database

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