Bilirubin-induced ER stress contributes to the inflammatory response and apoptosis in neuronal cells
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F17%3A10359712" target="_blank" >RIV/00216208:11110/17:10359712 - isvavai.cz</a>
Alternative codes found
RIV/00064165:_____/17:10359712
Result on the web
<a href="http://dx.doi.org/10.1007/s00204-016-1835-3" target="_blank" >http://dx.doi.org/10.1007/s00204-016-1835-3</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s00204-016-1835-3" target="_blank" >10.1007/s00204-016-1835-3</a>
Alternative languages
Result language
angličtina
Original language name
Bilirubin-induced ER stress contributes to the inflammatory response and apoptosis in neuronal cells
Original language description
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 NFDB 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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30103 - Neurosciences (including psychophysiology)
Result continuities
Project
<a href="/en/project/LH%2015097" target="_blank" >LH 15097: Molecular Basis of Bilirubin Neurotoxicity</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2017
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Archives of Toxicology
ISSN
0340-5761
e-ISSN
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Volume of the periodical
91
Issue of the periodical within the volume
4
Country of publishing house
DE - GERMANY
Number of pages
12
Pages from-to
1847-1858
UT code for WoS article
000398819200023
EID of the result in the Scopus database
2-s2.0-84984820645