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Bilirubin-induced ER stress contributes to the inflammatory response and apoptosis in neuronal cells
M. Qaisiya, C. Brischetto, J. Jašprová, L. Vitek, C. Tiribelli, C. Bellarosa,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články
NLK
ProQuest Central
od 2002-01-01 do Před 1 rokem
Medline Complete (EBSCOhost)
od 2000-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2002-01-01 do Před 1 rokem
Public Health Database (ProQuest)
od 2002-01-01 do Před 1 rokem
- MeSH
- apoptóza MeSH
- astrocytom metabolismus MeSH
- bilirubin metabolismus MeSH
- buněčná diferenciace MeSH
- fenylbutyráty farmakologie MeSH
- interleukin-8 metabolismus MeSH
- kaspasa 3 metabolismus MeSH
- lidé MeSH
- myši knockoutované MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- neuroblastom metabolismus MeSH
- neurony metabolismus patologie MeSH
- stres endoplazmatického retikula * MeSH
- transkripční faktor CHOP genetika MeSH
- umlčování genů MeSH
- viabilita buněk MeSH
- zánět patologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Unconjugated bilirubin (UCB) in newborns may lead to bilirubin neurotoxicity. Few studies investigated the activation of endoplasmic reticulum stress (ER stress) by UCB. We performed an in vitro comparative study using undifferentiated SH-SY5Y, differentiated GI-ME-N neuronal cells and human U87 astrocytoma cells. ER stress and its contribution to inflammation and apoptosis induced by UCB were analyzed. Cytotoxicity, ER stress and inflammation were observed only in neuronal cells, despite intracellular UCB accumulation in all three cell types. UCB toxicity was enhanced in undifferentiated SH-SY5Y cells and correlated with a higher mRNA expression of pro-apoptotic CHOP. Mouse embryonic fibroblast knockout for CHOP and CHOP siRNA-silenced SH-SY5Y increased cells viability upon UCB exposure. In SH-SY5Y, ER stress inhibition by 4-phenylbutyric acid reduced UCB-induced apoptosis and decreased the cleaved forms of caspase-3 and PARP proteins. Reporter gene assay and PERK siRNA showed that IL-8 induction by UCB is transcriptionally regulated by NFкB and PERK signaling. These data suggest that ER stress has an important role in the UCB-induced inflammation and apoptosis, and that targeting ER stress may represent a potential therapeutic approach to decrease UCB-induced neurotoxicity.
Citace poskytuje Crossref.org
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- $a Unconjugated bilirubin (UCB) in newborns may lead to bilirubin neurotoxicity. Few studies investigated the activation of endoplasmic reticulum stress (ER stress) by UCB. We performed an in vitro comparative study using undifferentiated SH-SY5Y, differentiated GI-ME-N neuronal cells and human U87 astrocytoma cells. ER stress and its contribution to inflammation and apoptosis induced by UCB were analyzed. Cytotoxicity, ER stress and inflammation were observed only in neuronal cells, despite intracellular UCB accumulation in all three cell types. UCB toxicity was enhanced in undifferentiated SH-SY5Y cells and correlated with a higher mRNA expression of pro-apoptotic CHOP. Mouse embryonic fibroblast knockout for CHOP and CHOP siRNA-silenced SH-SY5Y increased cells viability upon UCB exposure. In SH-SY5Y, ER stress inhibition by 4-phenylbutyric acid reduced UCB-induced apoptosis and decreased the cleaved forms of caspase-3 and PARP proteins. Reporter gene assay and PERK siRNA showed that IL-8 induction by UCB is transcriptionally regulated by NFкB and PERK signaling. These data suggest that ER stress has an important role in the UCB-induced inflammation and apoptosis, and that targeting ER stress may represent a potential therapeutic approach to decrease UCB-induced neurotoxicity.
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