KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL a Petr VAŇHARA. ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium. In 12th International Congress of Cell Biology, Programme & Abstract Book. 2016.
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Základní údaje
Originální název ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
Název anglicky ER Stress Modulates Senescence and EMT in Ovarian Surface Epithelium
Autoři KRATOCHVÍLOVÁ, Kateřina, Lukáš MORÁŇ, Cristina FONT CALVARONS, Ivana BALTASOVÁ, Aleš HAMPL a Petr VAŇHARA.
Vydání 12th International Congress of Cell Biology, Programme & Abstract Book, 2016.
Další údaje
Typ výsledku Konferenční abstrakt
Utajení není předmětem státního či obchodního tajemství
WWW URL
Klíčová slova česky stres endoplazmatického retikula, senescence, ovariální epitel, epiteliálně-mezenchymální tranzice
Klíčová slova anglicky endoplasmic reticulum stress, ER stress, UPR, senescence, ovarian surface epithelium, epithelial-to-mesenchymal transition, EMT
Příznaky Mezinárodní význam
Změnil Změnila: Mgr. Kateřina Vašíčková, Ph.D., učo 356999. Změněno: 29. 7. 2016 10:35.
Anotace
Endoplasmic reticulum (ER) is a multifunctional organelle primarily responsible for protein synthesis and folding. Disruption of ER function triggers a protective machinery called the unfolded protein response (UPR). UPR pathways then arrest the RNA translation and increase the production of ER chaperones to alleviate ER stress, or, if the stress cannot be resolved, UPR induces phenotypic change and/or apoptosis. Cellular senescence is a complex cell phenotype, whereby cells irreversibly cease to divide after a number of passages. It can be induced by telomere shortening, DNA damage, oxidative stress and activation of some oncogenes. Senescent cells accumulate with age in tissues and are assumed to play a role in age-associated diseases, such as Alzheimer disease or cancer. In our work, induction of senescence lead to upregulation of UPR hallmark proteins and interestingly, alleviation of ER stress by inhibition of UPR signaling or by chemical chaperons, overridden the onset of senescence. In summary, these results indicate a biologically relevant link between UPR and senescence of OSE cells that may contribute to better understanding of ovarian pathologies extending the portfolio of druggable molecular targets.
Anotace anglicky
Endoplasmic reticulum (ER) is a multifunctional organelle primarily responsible for protein synthesis and folding. Disruption of ER function triggers a protective machinery called the unfolded protein response (UPR). UPR pathways then arrest the RNA translation and increase the production of ER chaperones to alleviate ER stress, or, if the stress cannot be resolved, UPR induces phenotypic change and/or apoptosis. Cellular senescence is a complex cell phenotype, whereby cells irreversibly cease to divide after a number of passages. It can be induced by telomere shortening, DNA damage, oxidative stress and activation of some oncogenes. Senescent cells accumulate with age in tissues and are assumed to play a role in age-associated diseases, such as Alzheimer disease or cancer. In our work, induction of senescence lead to upregulation of UPR hallmark proteins and interestingly, alleviation of ER stress by inhibition of UPR signaling or by chemical chaperons, overridden the onset of senescence. In summary, these results indicate a biologically relevant link between UPR and senescence of OSE cells that may contribute to better understanding of ovarian pathologies extending the portfolio of druggable molecular targets.
VytisknoutZobrazeno: 24. 7. 2021 10:59