Abstract：
BACKGROUND:The inhalation of silicon dioxide (SiO2) particles causes silicosis, a stubborn pulmonary disease that is characterized by alveolar inflammation during the early stage. Soluble cytokine receptors (SCRs) play important roles in regulating inflammation by either attenuating or promoting cytokine signaling. However, the role of SCRs in silicosis remains unknown. METHODS AND RESULTS:Luminex assays revealed increased soluble vascular endothelial growth factor receptor (sVEGFR) family levels in the plasma of silicosis patients. In an enzyme-linked immunosorbent assay (ELISA), cells from the differentiated human monocytic cell line U937 released sVEGFR family proteins after exposure to SiO2 (50μg/cm2). Further Western blot experiments revealed that VEGFR expression was also elevated in U937 cells. In contrast, levels of sVEGFR family members did not change in the supernatants of human umbilical vein endothelial cells (HUVECs) after exposure to SiO2 (50μg/cm2). Interestingly, VEGFR expression in HUVECs decreased after SiO2 treatment. In a scratch assay, HUVECs exhibited cell migration ability, indicating the acquisition of mesenchymal properties. CONCLUSION:Our findings highlight the important role of sVEGFRs in both inflammation and fibrosis induced by SiO2, suggesting a possible mechanism for the fibrogenic effects observed in pulmonary diseases associated with fibrosis.
journal_name
Respir Physiol Neurobioljournal_title
Respiratory physiology & neurobiologyauthors
Chao J,Lv Y,Chen J,Wang J,Yao Hdoi
10.1016/j.resp.2017.08.015subject
Has Abstractpub_date
2018-01-01 00:00:00pages
1-8eissn
1569-9048issn
1878-1519pii
S1569-9048(17)30169-6journal_volume
247pub_type
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