Detailed Information on Publication Record
2018
Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium
VAŠÍČKOVÁ, Kateřina, Lukáš MORÁŇ, Dominik GURÍN and Petr VAŇHARABasic 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
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10601 Cell biology
Country of publisher
United States of America
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 3.360
RIV identification code
RIV/00216224:14110/18:00105151
Organization unit
Faculty of Medicine
UT WoS
000452397100019
Keywords in English
Ovarian surface epithelium; Endoplasmic reticulum stress; Unfolded protein response; Senescence; Tauroursodeoxycholic acid
Tags
International impact, Reviewed
Změněno: 9/2/2019 20:13, Soňa Böhmová
Abstract
V originále
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 project |
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MUNI/A/1298/2017, interní kód MU |
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