Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells
Identifieur interne : 000439 ( Main/Exploration ); précédent : 000438; suivant : 000440Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells
Auteurs : Pavlína Šime Ková ; So A Marvanová ; Pavel Kulich ; Lucie Králiková ; Ji Ne A ; Ji Ina Procházková ; Miroslav MachalaSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells.
Url:
DOI: 10.3390/ijms20246310
PubMed: 31847237
PubMed Central: 6940800
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells.</p>
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<tree><noCountry><name sortKey="Kralikova, Lucie" sort="Kralikova, Lucie" uniqKey="Kralikova L" first="Lucie" last="Králiková">Lucie Králiková</name>
<name sortKey="Kulich, Pavel" sort="Kulich, Pavel" uniqKey="Kulich P" first="Pavel" last="Kulich">Pavel Kulich</name>
<name sortKey="Machala, Miroslav" sort="Machala, Miroslav" uniqKey="Machala M" first="Miroslav" last="Machala">Miroslav Machala</name>
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<name sortKey="Prochazkova, Ji Ina" sort="Prochazkova, Ji Ina" uniqKey="Prochazkova J" first="Ji Ina" last="Procházková">Ji Ina Procházková</name>
<name sortKey="Sime Kova, Pavlina" sort="Sime Kova, Pavlina" uniqKey="Sime Kova P" first="Pavlína" last="Šime Ková">Pavlína Šime Ková</name>
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</affiliations>
</record>
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