J 2018

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

VAŠÍČKOVÁ, Kateřina, Lukáš MORÁŇ, Dominik GURÍN and Petr VAŇHARA

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

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

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
Name: Centrum analýz a modelování tkání a orgánů
MUNI/A/1298/2017, interní kód MU
Name: Zdroje pro tkáňové inženýrství 8 (Acronym: TissueEng 8)
Investor: Masaryk University, Category A