Role of SOD3 in silica-related lung fibrosis and pulmonary vascular remodeling.
Publication/Presentation Date
11-20-2018
Abstract
BACKGROUND: Work-place exposure to silica dust may lead to progressive lung inflammation culminating in the development of silicosis, an irreversible condition that can be complicated by onset of pulmonary hypertension (PH). The molecular mechanisms leading to the development of PH and lung fibrosis in response to silica are not well understood. Oxidant/antioxidant imbalance in the lung may promote fibroproliferation and vascular smooth muscle proliferation, ultimately leading to the development of PH. Herein, we analyze the development of PH and lung fibrosis in mice deficient in extracellular superoxide dismutase (SOD3), an enzyme with anti-oxidant activity.
METHODS: PH and silicosis were induced in wild-type and Sod3
RESULTS: C57BL6 mice exposed to silica showed attenuated expression of Sod3 in the lung suggesting a protective role for Sod3. Consistent with this, Sod3
CONCLUSIONS: Our data suggest that Sod3 and extracellular oxidative stress may play an important role in the development of pneumoconiosis and pulmonary vascular remodeling following exposure to environmental and occupational silica.
Volume
19
Issue
1
First Page
221
Last Page
221
ISSN
1465-993X
Published In/Presented At
Zelko, I. N., Zhu, J., & Roman, J. (2018). Role of SOD3 in silica-related lung fibrosis and pulmonary vascular remodeling. Respiratory research, 19(1), 221. https://doi.org/10.1186/s12931-018-0933-6
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
30453980
Department(s)
Administration and Leadership
Document Type
Article