Crystalline Silica Promotes Rat Fibrocyte Differentiation in Vitro,and Fibrocytes Participate in Silicosis in Vivo

Objective The aim of this study was to investigate the effects of Si O2 on fibrocytes and whether fibrocytes participate in silicosis in vivo. Methods A macrophagocyte（AM）/fibrocyte coculture system was established, and AMs were treated with 100 μg/mL SiO 2. Flow cytometry was used to detect the number of fibrocytes. Real‐time PCR was performed to measure the expression of collagen I, collagen III, and α‐SMA mR NA. The levels of collagen I, collagen III, and TGF‐β1 protein were determined by ELISA. Immunohistochemical staining was performed to measure α‐SMA protein expression. A rat silicosis model was induced by intratracheal instillation of SiO 2. Lung histopathological evaluation was conducted using HE and Masson＇s trichrome staining after 1 and 9 weeks. The number of fibrocytes in peripheral blood or lung tissue of rat was detected by flow cytometry. Double‐color immunofluorescence was applied to identify fibrocytes in the lung tissue. Results Peripheral blood monocytes were found to differentiate into fibrocytes in vitro in a time‐dependent manner, and exposure to crystalline silica might potentiate fibrocyte differentiation. In addition, fibrocytes were able to migrate from peripheral blood to the lung tissue, and the number of fibrocytes was increased after SiO 2 exposure. Conclusion Silica exposure potentiates fibrocyte differentiation, and fibrocytes may participate in silicosis in vivo.

Expression level of miR-155 in peripheral blood

Objective:To investigate the relationship between the expression level of miR-155 and the severity of coronary lesion,and explore the action mechanism.Methods:Peripheral blood mononuclear cells(PBMC) were isolated form blood simple from patients with acute myocardial infarction(AMI),unstable angina(UAP).stable angina(SAP) and chesl pain syndrome(CPS).RT-PCR was performed to analysis the expression level of miR-155 in peripheral blood mononuclear cells,plasma and RAW264.7 macrophagocyte.MTT was used to analyze the cell viability of OxLDL treated RAW264.7 macrophagocyte.Results:The expression level of miR-155 in blood sample from coronary heart disease patients was much lower than in the blood sample of non-coronary heart disease(P<0.05).The level of miR-155 in PBMCs was much higher in the blood sample from CPS group than the other three group,and the level of miR-155 in plasma was higher in the CPS group than in the UAP and the AMI group,the difference was statistically significant(P<0.05).The expression level of miR-155 in PBMCs is positively associated with the level in the plasma(r=0.861,P=0.000).OxLDL can induce the expression of miR-155 in RAW264.7 macrophagocyte.decrease the cell viability of RAW264.7 macrophagocyte.and with the concentration and the treatment time of OxLDL increased,the effort become more obvious.The inhibition effort of OxLDL to RAW264.7macrophagocyte with high miR-155 expression is much lower than the control group,and it is statistically significant after treated for 12.24 and 48 h.Conclusions:miR-155 plays a protective role in the progression of atherosclerosis,and it may be achieved by reducing the apoptosis effort of OxLDL to RAW264.7 macrophagocyte.