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

Kód výsledku v 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>

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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

Název v anglickém jazyce

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

Popis výsledku anglicky

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

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

<a href="/cs/project/GA15-13732S" target="_blank" >GA15-13732S: Molekulární podstata erytroidního defektu a narušené utilizace železa u deficitu DMT1 a u Diamondovy-Blackfanovy anémie</a><br>

Návaznosti

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

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Journal of Molecular Medicine

ISSN

0946-2716

e-ISSN

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Svazek periodika

93

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

10

Strana od-do

857-866

Kód UT WoS článku

000358326500005

EID výsledku v databázi Scopus

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