p38 MAPK is activated but does not play a key role during apoptosis induction by saturated fatty acid in human pancreatic β-cells

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F16%3A43911020" target="_blank" >RIV/00216208:11120/16:43911020 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.3390/ijms17020159" target="_blank" >http://dx.doi.org/10.3390/ijms17020159</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/ijms17020159" target="_blank" >10.3390/ijms17020159</a>

Result language

angličtina

Original language name

p38 MAPK is activated but does not play a key role during apoptosis induction by saturated fatty acid in human pancreatic β-cells

Original language description

Saturated stearic acid (SA) induces apoptosis in the human pancreatic β-cells NES2Y. However, the molecular mechanisms involved are unclear. We showed that apoptosis-inducing concentrations of SA activate the p38 MAPK signaling pathway in these cells. Therefore, we tested the role of p38 MAPK signaling pathway activation in apoptosis induction by SA in NES2Y cells. Crosstalk between p38 MAPK pathway activation and accompanying ERK pathway inhibition after SA application was also tested. The inhibition of p38 MAPK expression by siRNA silencing resulted in a decrease in MAPKAPK-2 activation after SA application, but it had no significant effect on cell viability or the level of phosphorylated ERK pathway members. The inhibition of p38 MAPK activity by the specific inhibitor SB202190 resulted in inhibition of MAPKAPK-2 activation and noticeable activation of ERK pathway members after SA treatment but in no significant effect on cell viability. p38 MAPK overexpression by plasmid transfection produced an increase in MAPKAPK-2 activation after SA exposure but no significant influence on cell viability or ERK pathway activation. The activation of p38 MAPK by the specific activator anisomycin resulted in significant activation of MAPKAPK-2. Concerning the effect on cell viability, application of the activator led to apoptosis induction similar to application of SA (PARP cleavage and caspase-7, -8, and -9 activation) and in inhibition of ERK pathway members. We demonstrated that apoptosis-inducing concentrations of SA activate the p38 MAPK signaling pathway and that this activation could be involved in apoptosis induction by SA in the human pancreatic β-cells NES2Y. However, this involvement does not seem to play a key role. Crosstalk between p38 MAPK pathway activation and ERK pathway inhibition in NES2Y cells seems likely. Thus, the ERK pathway inhibition by p38 MAPK activation does not also seem to be essential for SA-induced apoptosis.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

EB - Genetics and molecular biology

OECD FORD branch

—

Project

<a href="/en/project/GP14-00630P" target="_blank" >GP14-00630P: Regulation of apoptosis induction by saturated and unsaturated fatty acids in pancreatic beta-cells: a proteomic approach</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2016

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

International Journal of Molecular Sciences

ISSN

1422-0067

e-ISSN

—

Volume of the periodical

17

Issue of the periodical within the volume

2

Country of publishing house

CH - SWITZERLAND

Number of pages

15

Pages from-to

"Article 159"

UT code for WoS article

000371830800080

EID of the result in the Scopus database

2-s2.0-84957596359