Ultrafine particles translocate to the central nervous system and activate oxidative stress-related pathways. The transcription factor Nrf2 activation by ERK1-2 has been suggested as a key regulator of cellular response to oxidative stress.C6 glioma cells have been treated with different doses of diesel exhaust particles (25 μg/ml, DEP25, and 50 μg/ml, DEP50), for different times. Cells have been screened for oxidative stress and inflammatory markers, and for the activation of the MEK-ERK1-2 pathway. The same markers have been examined after inhibition of MEK, the kinase upstream to ERK1-2.3 h and 24 h of DEP25 and DEP50 induced a significant increase in HO-1 levels. After 24 h, DEP25 and DEP50 induced an increase in HO-1 and Cyp1b1 levels, while increase in OGG1 level was observed only with DEP25.After 5 h of treatment with DEP25, ERK1-2 resulted phosphorylated, concomitantly with a significant increase in HO-1 levels, no changes in iNOS levels, and decreased levels of anti-oxidant enzymes. After treatment with MEK inhibitor U0126, ERK1-2 showed no activation, with a consequent decrease in Nrf2, no increase in HO-1 and a significant increase of iNOS. MEK inhibitor is able to deplete anti-oxidant enzymes.In conclusion, the MEK-ERK1-2 pathway is involved in regulating the anti-oxidant strategies to compensate the oxidative status induced by DEP treatment.

Farina, F., Milani, C., Botto, L., Lonati, E., Bulbarelli, A., Palestini, P. (2016). Involvement of MEK-ERK1-2 pathway in the anti-oxidant response in C6 glioma cells after diesel exhaust particles exposure. TOXICOLOGY LETTERS, 250-251(250-251), 57-65 [10.1016/j.toxlet.2016.04.008].

Involvement of MEK-ERK1-2 pathway in the anti-oxidant response in C6 glioma cells after diesel exhaust particles exposure

FARINA, FRANCESCA
Primo
;
MILANI, CHIARA
Secondo
;
BOTTO, LAURA MARIA;LONATI, ELENA RITA;BULBARELLI, ALESSANDRA
Penultimo
;
PALESTINI, PAOLA NOVERINA ADA
Ultimo
2016

Abstract

Ultrafine particles translocate to the central nervous system and activate oxidative stress-related pathways. The transcription factor Nrf2 activation by ERK1-2 has been suggested as a key regulator of cellular response to oxidative stress.C6 glioma cells have been treated with different doses of diesel exhaust particles (25 μg/ml, DEP25, and 50 μg/ml, DEP50), for different times. Cells have been screened for oxidative stress and inflammatory markers, and for the activation of the MEK-ERK1-2 pathway. The same markers have been examined after inhibition of MEK, the kinase upstream to ERK1-2.3 h and 24 h of DEP25 and DEP50 induced a significant increase in HO-1 levels. After 24 h, DEP25 and DEP50 induced an increase in HO-1 and Cyp1b1 levels, while increase in OGG1 level was observed only with DEP25.After 5 h of treatment with DEP25, ERK1-2 resulted phosphorylated, concomitantly with a significant increase in HO-1 levels, no changes in iNOS levels, and decreased levels of anti-oxidant enzymes. After treatment with MEK inhibitor U0126, ERK1-2 showed no activation, with a consequent decrease in Nrf2, no increase in HO-1 and a significant increase of iNOS. MEK inhibitor is able to deplete anti-oxidant enzymes.In conclusion, the MEK-ERK1-2 pathway is involved in regulating the anti-oxidant strategies to compensate the oxidative status induced by DEP treatment.
Articolo in rivista - Articolo scientifico
Anti-oxidant proteins; Diesel exhaust particles; ERK1-2; HO-1; Nrf2; Oxidative stress;
ERK1-2; HO-1; Nrf2; anti-oxidant proteins; diesel exhaust particles; oxidative stress
English
apr-2016
2016
250-251
250-251
57
65
reserved
Farina, F., Milani, C., Botto, L., Lonati, E., Bulbarelli, A., Palestini, P. (2016). Involvement of MEK-ERK1-2 pathway in the anti-oxidant response in C6 glioma cells after diesel exhaust particles exposure. TOXICOLOGY LETTERS, 250-251(250-251), 57-65 [10.1016/j.toxlet.2016.04.008].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/109668
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