Proteomic analysis of proteins from bronchoalveolar lavage fluid reveals the action mechanism of ultrafine carbon black-induced lung injury in mice.
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 alpha2-macroglobulin (alpha2M) 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.
Chang
Chih-Ching
CC
Department of Environmental and Occupational Health, National Cheng Kung University, Tainan, Taiwan.
Chen
Shu-Hui
SH
Ho
Shih-Hsin
SH
Yang
Chun-Yuh
CY
Wang
Hong-Da
HD
Tsai
Mei-Ling
ML
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000166:cytology; D045744:Cell Line, Tumor; D002570:Ceruloplasmin / Q000032:analysis / Q000378:metabolism; D004591:Electrophoresis, Polyacrylamide Gel; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D066246:ErbB Receptors / Q000032:analysis / Q000378:metabolism; D006801:Humans; D053680:Leukemia Inhibitory Factor Receptor alpha Subunit / Q000032:analysis / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010316:Particle Size; D020543:Proteome / Q000032:analysis* / Q000378:metabolism; D040901:Proteomics / Q000379:methods*; D012709:Serum Albumin / Q000032:analysis / Q000378:metabolism; D053260:Soot / Q000008:administration & dosage / Q000737:chemistry / Q000633:toxicity; D021241:Spectrometry, Mass, Electrospray Ionization; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000378:metabolism
D053680:Leukemia Inhibitory Factor Receptor alpha Subunit; C507841:Lifr protein, mouse; D020543:Proteome; D012709:Serum Albumin; D053260:Soot; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D002570:Ceruloplasmin; D066246:ErbB Receptors