Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F18%3A00105151" target="_blank" >RIV/00216224:14110/18:00105151 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/18:00071775

Výsledek na webu

<a href="http://dx.doi.org/10.1007/s00441-018-2888-9" target="_blank" >http://dx.doi.org/10.1007/s00441-018-2888-9</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00441-018-2888-9" target="_blank" >10.1007/s00441-018-2888-9</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium

Popis výsledku v původním jazyce

Ovarian surface epithelium (OSE) forms a single layer of mostly cuboidal cells on surface of mammalian ovaries that is inherently exposed to cell stress evoked by tissue damage every ovulation and declines morphologically after menopause. Endoplasmic reticulum (ER) is a principal cell organelle involved in proteosynthesis, but also integrating various stress signals. ER stress evokes a conserved signaling pathway, the unfolded protein response (UPR), leading to cell death or adaptation to stress conditions. In this work, we document that mouse OSE suffers from ER stress during replicative senescence in vitro, develops abnormalities in ER and initiates UPR. Attenuation of ER stress in senescent OSE by tauroursodeoxycholic acid (TUDCA) reconditions ER architecture and leads to delayed onset of senescence. In summary, we show for the first time a mutual molecular link between ER stress response and replicative senescence leading to phenotypic changes of non-malignant ovarian surface epithelium.

Název v anglickém jazyce

Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium

Popis výsledku anglicky

Ovarian surface epithelium (OSE) forms a single layer of mostly cuboidal cells on surface of mammalian ovaries that is inherently exposed to cell stress evoked by tissue damage every ovulation and declines morphologically after menopause. Endoplasmic reticulum (ER) is a principal cell organelle involved in proteosynthesis, but also integrating various stress signals. ER stress evokes a conserved signaling pathway, the unfolded protein response (UPR), leading to cell death or adaptation to stress conditions. In this work, we document that mouse OSE suffers from ER stress during replicative senescence in vitro, develops abnormalities in ER and initiates UPR. Attenuation of ER stress in senescent OSE by tauroursodeoxycholic acid (TUDCA) reconditions ER architecture and leads to delayed onset of senescence. In summary, we show for the first time a mutual molecular link between ER stress response and replicative senescence leading to phenotypic changes of non-malignant ovarian surface epithelium.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/EE2.3.20.0185" target="_blank" >EE2.3.20.0185: Centrum analýz a modelování tkání a orgánů</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

CELL AND TISSUE RESEARCH

ISSN

0302-766X

e-ISSN

—

Svazek periodika

374

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

643-652

Kód UT WoS článku

000452397100019

EID výsledku v databázi Scopus

2-s2.0-85052148206