It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Diesel exhaust particles (DEP) are known to generate reactive oxygen species in the respiratory system, triggering cells to activate antioxidant defence mechanisms, such as Keap1-Nrf2 signalling and autophagy. The aim of this study was to investigate the relationship between the Keap1-Nrf2 signalling and autophagy pathways after DEP exposure. BEAS-2B cells were transfected with silencing RNA (siRNA) specific to Nrf2 and exposed to DEP. The relative levels of mRNA for Nrf2, NQO1, HO-1, LC3B, p62 and Atg5 were determined using RT-PCR, while the levels of LCB3, Nrf2, and p62 protein were determined using Western blotting. The autophagy inhibitor bafilomycin caused a significant decrease in the production of Nrf2, HO-1 and NQO1 compared to DEPs treatment, whereas the Nrf2 activator sulforaphane increased the LC3B (p = 0.020) levels. BEAS-2B cells exposed to DEP at a concentration of 50 μg/mL for 2 h showed a significant increase in the expression of LC3B (p = 0.001), p62 (p = 0.008), Nrf2 (p = 0.003), HO-1 (p = 0.001) and NQO1 (p = 0.015) genes compared to control. In siRNA-transfected cells, the LC3B (p < 0.001), p62 (p = 0.001) and Atg5 (p = 0.024) mRNA levels and the p62 and LC3II protein levels were decreased, indicating that Nrf2 modulated the expression of autophagy markers (R < 1). These results imply that, in bronchial cells exposed to DEP, the Nrf2 system positively regulates autophagy to maintain cellular homeostasis.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Laboratory of Experimental Air Pollution (LIM-05), Department of Pathology, School of Medicine, University of São Paulo, Av. Dr. Arnaldo 455, São Paulo, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
2 Laboratory of Investigation in Ophthalmology (LIM-33), Division of Ophthalmology, School of Medicine, University of São Paulo, Av. Dr. Arnaldo 455, São Paulo, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
3 Center for Translational Research in Oncology (LIM24), Cancer Institute of the State of São Paulo, Hospital das Clínicas (HCFMUSP) School of Medicine, University of São Paulo, Av. Dr. Arnaldo, 251, São Paulo, SP, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
4 Rheumatology Division of the Hospital das Clinicas da Faculdade de Medicina da Universidade de Sao Paulo FMUSP, São Paulo, SP, BR, Av. Dr. Arnaldo, 455, room 3124, Cerqueira César, São Paulo, SP, Brazil (GRID:grid.11899.38)
5 Chemistry Institute, University of São Paulo, São Paulo, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
6 Physicist. Researcher of clean energy alternatives and clean mobility. Inventor and freelancer of Laboratory of Experimental Air Pollution in University of São Paulo, São Paulo, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)