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Apocynin and Diphenyleneiodonium Induce Oxidative Stress and Modulate PI3K/Akt and MAPK/Erk Activity in Mouse Embryonic Stem Cells
J. Kučera, L. Binó, K. Štefková, J. Jaroš, O. Vašíček, J. Večeřa, L. Kubala, J. Pacherník,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 2008
PubMed Central
from 2008
Europe PubMed Central
from 2008
ProQuest Central
from 2014-01-01
Open Access Digital Library
from 2008-01-01
Open Access Digital Library
from 2008-01-01
Open Access Digital Library
from 2009-01-01
Medline Complete (EBSCOhost)
from 2011-01-01
Health & Medicine (ProQuest)
from 2014-01-01
Wiley-Blackwell Open Access Titles
from 2008
PubMed
26788250
DOI
10.1155/2016/7409196
Knihovny.cz E-resources
- MeSH
- Acetophenones pharmacology MeSH
- Extracellular Signal-Regulated MAP Kinases metabolism MeSH
- Phosphatidylinositol 3-Kinases metabolism MeSH
- Phosphorylation drug effects MeSH
- Mouse Embryonic Stem Cells drug effects metabolism MeSH
- Mice MeSH
- NADPH Oxidases genetics metabolism MeSH
- Onium Compounds pharmacology MeSH
- Oxidative Stress drug effects MeSH
- Cell Proliferation drug effects MeSH
- Wnt Proteins metabolism MeSH
- Proto-Oncogene Proteins c-akt metabolism MeSH
- Reactive Oxygen Species metabolism MeSH
- Drug Synergism MeSH
- STAT3 Transcription Factor metabolism MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Reactive oxygen species (ROS) are important regulators of cellular functions. In embryonic stem cells, ROS are suggested to influence differentiation status. Regulated ROS formation is catalyzed primarily by NADPH-dependent oxidases (NOXs). Apocynin and diphenyleneiodonium are frequently used inhibitors of NOXs; however, both exhibit uncharacterized effects not related to NOXs inhibition. Interestingly, in our model of mouse embryonic stem cells we demonstrate low expression of NOXs. Therefore we aimed to clarify potential side effects of these drugs. Both apocynin and diphenyleneiodonium impaired proliferation of cells. Surprisingly, we observed prooxidant activity of these drugs determined by hydroethidine. Further, we revealed that apocynin inhibits PI3K/Akt pathway with its downstream transcriptional factor Nanog. Opposite to this, apocynin augmented activity of canonical Wnt signaling. On the contrary, diphenyleneiodonium activated both PI3K/Akt and Erk signaling pathways without affecting Wnt. Our data indicates limits and possible unexpected interactions of NOXs inhibitors with intracellular signaling pathways.
References provided by Crossref.org
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