Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic ?-cells
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F13%3A43907087" target="_blank" >RIV/00216208:11120/13:43907087 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1159/000343367" target="_blank" >http://dx.doi.org/10.1159/000343367</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1159/000343367" target="_blank" >10.1159/000343367</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic ?-cells
Popis výsledku v původním jazyce
Background: Fatty acid-induced apoptosis and ER stress of pancreatic ?-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 suggestedER stress mediator JNK in saturated fatty acid-induced apoptosis of the human pancreatic ?-cells NES2Y. Results: We found that stearic acid at apoptosis-inducing concentration activated ER stress signaling pathways, i.e. IRE1?, PERK and ATF6 pathways, inNES2Y 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
Název v anglickém jazyce
Caspase-2 and JNK activated by saturated fatty acids are not involved in apoptosis induction but modulate ER stress in human pancreatic ?-cells
Popis výsledku anglicky
Background: Fatty acid-induced apoptosis and ER stress of pancreatic ?-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 suggestedER stress mediator JNK in saturated fatty acid-induced apoptosis of the human pancreatic ?-cells NES2Y. Results: We found that stearic acid at apoptosis-inducing concentration activated ER stress signaling pathways, i.e. IRE1?, PERK and ATF6 pathways, inNES2Y 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
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
FB - Endokrinologie, diabetologie, metabolismus, výživa
OECD FORD obor
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Návaznosti výsledku
Projekt
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Návaznosti
S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2013
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Cellular Physiology and Biochemistry
ISSN
1015-8987
e-ISSN
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Svazek periodika
31
Číslo periodika v rámci svazku
2-3
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
13
Strana od-do
277-289
Kód UT WoS článku
000318411800009
EID výsledku v databázi Scopus
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