Diesel Exhaust Particulates Affect Cell Signaling, Mucin Profiles, and Apoptosis in Trachea Explants of Balb/C Mice

作者:Seriani Robson; Junqueira Mara de Souza; de Toledo Alessandra Choqueta; Martins Milton Arruda; Seckler Marcelo; Alencar Adriano Mesquita; Negri Elnara Marcia; Ferraz Silva Luiz Fernando; Mauad Thais; Nascimento Saldiva Paulo Hilario; Macchione Mariangela*
来源:Environmental Toxicology, 2015, 30(11): 1297-1308.
DOI:10.1002/tox.22000

摘要

Particulate matter from diesel exhaust (DEP) has toxic properties and can activate intracellular signaling pathways and induce metabolic changes. This study was conducted to evaluate the activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) and to analyze the mucin profile (acid (AB(+)), neutral (PAS(+)), or mixed (AB/PAS(+)) mucus) and vacuolization (V) of tracheal explants after treatment with 50 or 100 mu g/mL DEP for 30 or 60 min. Western blot analyses showed small increases in ERK1/2 and JNK phosphorylation after 30 min of 100 mu g/mL DEP treatment compared with the control. An increase in JNK phosphorylation was observed after 60 min of treatment with 50 mu g/mL DEP compared with the control. We did not observe any change in the level of ERK1/2 phosphorylation after treatment with 50 mu g/mL DEP. Other groups of tracheas were subjected to histological sectioning and stained with periodic acid-Schiff (PAS) reagent and Alcian Blue (AB). The stained tissue sections were then subjected to morphometric analysis. The results obtained were compared using ANOVA. Treatment with 50 mu g/mL DEP for 30 min or 60 min showed a significant increase (p< 0.001) in the amount of acid mucus, a reduction in neutral mucus, a significant reduction in mixed mucus, and greater vacuolization. Our results suggest that compounds found in DEPs are able to activate acid mucus production and enhance vacuolization and cell signaling pathways, which can lead to airway diseases.

  • 出版日期2015-11