VAŠÍČKOVÁ, Kateřina, Lukáš MORÁŇ, Dominik GURÍN and Petr VAŇHARA. Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium. CELL AND TISSUE RESEARCH. Heidelberg: Springer Verlag, 2018, vol. 374, No 3, p. 643-652. ISSN 0302-766X. Available from: https://dx.doi.org/10.1007/s00441-018-2888-9.
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Basic information
Original name Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium
Authors VAŠÍČKOVÁ, Kateřina (203 Czech Republic, belonging to the institution), Lukáš MORÁŇ (203 Czech Republic, belonging to the institution), Dominik GURÍN (203 Czech Republic) and Petr VAŇHARA (203 Czech Republic, guarantor, belonging to the institution).
Edition CELL AND TISSUE RESEARCH, Heidelberg, Springer Verlag, 2018, 0302-766X.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 3.360
RIV identification code RIV/00216224:14110/18:00105151
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1007/s00441-018-2888-9
UT WoS 000452397100019
Keywords in English Ovarian surface epithelium; Endoplasmic reticulum stress; Unfolded protein response; Senescence; Tauroursodeoxycholic acid
Tags 14110517, rivok
Tags International impact, Reviewed
Changed by Changed by: Soňa Böhmová, učo 232884. Changed: 9/2/2019 20:13.
Abstract
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.
Links
EE2.3.20.0185, research and development projectName: Centrum analýz a modelování tkání a orgánů
MUNI/A/1298/2017, interní kód MUName: Zdroje pro tkáňové inženýrství 8 (Acronym: TissueEng 8)
Investor: Masaryk University, Category A
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