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Proteomic analysis of proteins from bronchoalveolar lavage fluid reveals the action mechanism of ultrafine carbon black‐induced lung injury in mice
Author(s) -
Chang ChihChing,
Chen ShuHui,
Ho ShihHsin,
Yang ChunYuh,
Wang HongDa,
Tsai MeiLing
Publication year - 2007
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200700164
Subject(s) - bronchoalveolar lavage , western blot , leukemia inhibitory factor receptor , lung , chemistry , receptor , immunology , biology , medicine , cytokine , leukemia inhibitory factor , biochemistry , interleukin 6 , gene
Previous studies have shown that ultrafine carbon black (ufCB) could cause oxidative stress and lung injury, but the mechanisms have not been clearly demonstrated. In this study, 1‐D gel electrophoresis coupled with LC/MS/MS (1‐D geLC/MS/MS) was carried out with bronchoalveolar lavage fluid (BALF) to identify proteins associated with ufCB‐induced lung injury. If required, Western blot was conducted additionally to validate proteins. Thirty‐three proteins were identified, including leukemia inhibitory factor receptor (LIFR) and epidermal growth factor receptor (EGFR). Western blot analysis showed that ufCB exposure caused the increases of LIFR and EGFR in BALF and decreases of both receptors in lung tissues, suggesting the acceleration of epithelial shedding from the lung and increase of cell debris with membrane proteins EGFR and LIFR in BALF. There were strong correlations between vascular endothelial growth factor (VEGF) and albumin ( p <0.01) or α2‐macroglobulin (α2M) in BALF ( p <0.05). Importantly, antioxidant ceruloplasmin (Cp) was shown to be produced from lung epithelial cells in response to ufCB exposure. This is the first study to apply 1‐D ge LC/MS/MS and experimental studies to reveal the mechanisms involved in the pathogenesis of ufCB‐induced lung injury.