Cyclophilin A accelerates SiO2-induced macrophage foaming.

ABSTRACT

Silicosis is a common occupational disease characterized by lung inflammation, fibrosis and pulmonary dysfunction caused by long-term inhalation of free SiO2. Cell foaming and the change of CyPA have been observed in SiO2-induced macrophages, but the specific mechanism of CyPA in SiO2-induced foam cells remains poorly understood. The purpose of this study is to explore the mechanism of CyPA in SiO2-induced macrophage foaming and its effect on silicosis. We found that overexpression of CyPA promoted the macrophage foaming and the expression of COL I and α-SMA, while silencing CyPA inhibites the macrophage foaming and the expression of COL I and α-SMA. After blocking the expression of CD36 on the basis of overexpression CyPA, we found it inhibites the macrophage foaming. In conclusion, CyPA can affect the foaming of macrophages and may participate in silicosis fibrosis.