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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F13%3A43907087%21RIV14-MSM-11120___
rdf:type
skos:Concept n9:Vysledek
dcterms:description
Background: Fatty acid-induced apoptosis and ER stress of pancreatic β-cells contribute to the development of type 2 diabetes, however, the molecular mechanisms involved are unclear. Aims: In this study we have tested the role of caspase-2 and suggested ER stress mediator JNK in saturated fatty acid-induced apoptosis of the human pancreatic β-cells NES2Y. Results: We found that stearic acid at apoptosis-inducing concentration activated ER stress signaling pathways, i.e. IRE1α, PERK and ATF6 pathways, in NES2Y cells. During stearic acid-induced apoptosis, JNK inhibition did not decrease the rate of apoptosis nor the activation of caspase-8, -9, -7 and -2 and PARP cleavage. In addition, inhibition of JNK activity did not affect CHOP expression although it did decrease the induction of BiP expression after stearic acid treatment. Caspase-2 silencing had no effect on PARP as well as caspase-8, -9 and -7 cleavage and the induction of CHOP expression, however, it also decreased the induction of BiP expression. Surprisingly, caspase-2 silencing was accompanied by increased phosphorylation of c-Jun. Conclusions: We have demonstrated that caspase-2 as well as JNK are not key players in apoptosis induction by saturated fatty acids in human pancreatic β-cells NES2Y. However, they appear to be involved in the modulation of saturated fatty acid-induced ER stress signaling, probably by a mechanism independent of c-Jun phosphorylation. Background: Fatty acid-induced apoptosis and ER stress of pancreatic β-cells contribute to the development of type 2 diabetes, however, the molecular mechanisms involved are unclear. Aims: In this study we have tested the role of caspase-2 and suggested ER stress mediator JNK in saturated fatty acid-induced apoptosis of the human pancreatic β-cells NES2Y. Results: We found that stearic acid at apoptosis-inducing concentration activated ER stress signaling pathways, i.e. IRE1α, PERK and ATF6 pathways, in NES2Y cells. During stearic acid-induced apoptosis, JNK inhibition did not decrease the rate of apoptosis nor the activation of caspase-8, -9, -7 and -2 and PARP cleavage. In addition, inhibition of JNK activity did not affect CHOP expression although it did decrease the induction of BiP expression after stearic acid treatment. Caspase-2 silencing had no effect on PARP as well as caspase-8, -9 and -7 cleavage and the induction of CHOP expression, however, it also decreased the induction of BiP expression. Surprisingly, caspase-2 silencing was accompanied by increased phosphorylation of c-Jun. Conclusions: We have demonstrated that caspase-2 as well as JNK are not key players in apoptosis induction by saturated fatty acids in human pancreatic β-cells NES2Y. However, they appear to be involved in the modulation of saturated fatty acid-induced ER stress signaling, probably by a mechanism independent of c-Jun phosphorylation.
dcterms:title
Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic β-cells Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic β-cells
skos:prefLabel
Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic β-cells Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic β-cells
skos:notation
RIV/00216208:11120/13:43907087!RIV14-MSM-11120___
n9:predkladatel
n10:orjk%3A11120
n3:aktivita
n4:S n4:I
n3:aktivity
I, S
n3:cisloPeriodika
2-3
n3:dodaniDat
n15:2014
n3:domaciTvurceVysledku
n14:4220803 n14:7090277 n14:4215036 n14:1758330
n3:druhVysledku
n8:J
n3:duvernostUdaju
n18:S
n3:entitaPredkladatele
n13:predkladatel
n3:idSjednocenehoVysledku
64382
n3:idVysledku
RIV/00216208:11120/13:43907087
n3:jazykVysledku
n12:eng
n3:klicovaSlova
beta-cells; endoplasmic reticulum stress; apoptosis; saturated fatty acids; JNK; caspase-2
n3:klicoveSlovo
n11:caspase-2 n11:endoplasmic%20reticulum%20stress n11:apoptosis n11:beta-cells n11:saturated%20fatty%20acids n11:JNK
n3:kodStatuVydavatele
CH - Švýcarská konfederace
n3:kontrolniKodProRIV
[689C7C64BBFB]
n3:nazevZdroje
Cellular Physiology and Biochemistry
n3:obor
n19:FB
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
5
n3:rokUplatneniVysledku
n15:2013
n3:svazekPeriodika
31
n3:tvurceVysledku
Šrámek, Jan Němcová-Fürstová, Vlasta Balušíková, Kamila Kovář, Jan James, Roger F.
n3:wos
000318411800009
s:issn
1015-8987
s:numberOfPages
13
n16:doi
10.1159/000343367
n7:organizacniJednotka
11120