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Alleviation of endoplasmic reticulum stress by tauroursodeoxycholic acid delays senescence of mouse ovarian surface epithelium
K. Vašíčková, L. Moráň, D. Gurín, P. Vaňhara,
Language English Country Germany
Document type Journal Article
NLK
ProQuest Central
from 2000-12-01 to 1 year ago
Medline Complete (EBSCOhost)
from 2000-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 2000-12-01 to 1 year ago
Health & Medicine (ProQuest)
from 2000-12-01 to 1 year ago
- MeSH
- Down-Regulation drug effects MeSH
- Epithelium drug effects pathology ultrastructure MeSH
- Taurochenodeoxycholic Acid pharmacology MeSH
- RNA, Messenger genetics metabolism MeSH
- Mice MeSH
- Ovary pathology MeSH
- Cellular Senescence drug effects MeSH
- Endoplasmic Reticulum Stress drug effects MeSH
- Tunicamycin pharmacology MeSH
- Up-Regulation drug effects MeSH
- Telomere Shortening drug effects MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
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.
References provided by Crossref.org
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