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Cyclophilin A accelerates SiO2-induced macrophage foaming.
Heliang Liu1, Hailan He2, Ying Tian2
1School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, China; Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei 063210, China.
Cellular Signalling
|December 19, 2022
Summary
Cyclophilin A (CyPA) promotes macrophage foaming and fibrosis in silicosis. Blocking CD36 inhibits this foaming, suggesting CyPA’s role in silica-induced lung disease.
Area of Science:
- Occupational Medicine
- Immunology
- Cell Biology
Background:
- Silicosis, an occupational lung disease, results from silica (SiO2) inhalation.
- Macrophage foaming and changes in CyPA are noted in SiO2 exposure, but mechanisms are unclear.
Purpose of the Study:
- To investigate the mechanism of CyPA in silica-induced macrophage foaming.
- To determine CyPA's role in silicosis fibrosis.
Main Methods:
- Studied CyPA's effect on macrophage foaming and expression of COL I and α-SMA.
- Investigated the role of CD36 in CyPA-mediated macrophage foaming.
Main Results:
- Overexpression of CyPA enhanced macrophage foaming and COL I/α-SMA expression.
- Silencing CyPA inhibited macrophage foaming and COL I/α-SMA expression.
- Blocking CD36 reduced CyPA-induced macrophage foaming.
Conclusions:
- CyPA influences macrophage foaming and may contribute to silicosis fibrosis.
- CD36 is involved in the CyPA-mediated foaming process in silicosis.
