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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,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články
NLK
ProQuest Central
od 2000-12-01 do Před 1 rokem
Medline Complete (EBSCOhost)
od 2000-01-01 do Před 1 rokem
Nursing & Allied Health Database (ProQuest)
od 2000-12-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2000-12-01 do Před 1 rokem
- MeSH
- down regulace účinky léků MeSH
- epitel účinky léků patologie ultrastruktura MeSH
- kyselina taurochenodeoxycholová farmakologie MeSH
- messenger RNA genetika metabolismus MeSH
- myši MeSH
- ovarium patologie MeSH
- stárnutí buněk účinky léků MeSH
- stres endoplazmatického retikula účinky léků MeSH
- tunikamycin farmakologie MeSH
- upregulace účinky léků MeSH
- zkracování telomer účinky léků MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články 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.
Citace poskytuje Crossref.org
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