Objective To investigate the expression of mitochondrial autophagy-associated protein PINK1 and Parkin in parotid pleomorphic adenoma (PA) and carcinoma ex pleomorphic adenoma(CA-EX-PA). Methods The expression of PINK1 and Parkin were detected by immunohistochemistry in 24 cases of normal parotid gland tissues, 32 cases of PA tissues and 42 cases of CA-EX-PA tissues. The correlations of PINK1 and Parkin expression with the clinicopathologic characteristics of CA-EX-PA patients were analyzed. Results The positive rates of PINK1 in normal parotid gland, PA and CA-EX-PA tissues were 100%, 91% and 67% respectively; and those of Parkin were 100%, 88% and 52% respectively. The expression rates of PINK1 and Parkin in PA and CA-EX-PA tissues were significantly lower than those in normal tissues (P < 0.05). The expression of PINK1 and Parkin protein were positively correlated in CA-EX-PA tissues (r=0.877, P < 0.01). In CA-EX-PA tissues, the expression of PINK1 and Parkin were associated with tumor invasion, lymph node metastasis and TNM stage (P < 0.05). Conclusion The expression of PINK1 and Parkin are decreased in PA and CA-EX-PA tissues. The decrease of mitochondrial autophagy activity might play important roles in the development, invasion and metastasis of parotid gland tumors.

BACKGROUND:Human placental mesenchymal stem cells have been shown to be effective in inhibiting the development of pulmonary fibrosis,but the underlying mechanisms remain unclear. OBJECTIVE:To investigate the therapeutic effect and related mechanism of human placental mesenchymal stem cells on silica-induced pulmonary fibrosis in human embryonic lung fibroblasts(MRC-5). METHODS:CCK-8 assay was used to detect the effects of different mass concentrations of silica on the proliferation of MRC-5 at different time points.Immunofluorescence staining was used to screen out the best stimulating mass concentration and time of silica for subsequent experiments.MRC-5 cells were divided into blank group,silica group,and silica + human placental mesenchymal stem cell group.In the blank group,cells were not treated.In the silica group,MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours.In the silica + human placental mesenchymal stem cell group,MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours and then co-cultured with human placental mesenchymal stem cells for 24 hours.Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and collagen type I in cells of each group.Western blot assay was used to detect the expressions of pulmonary fibrosis-related proteins and TGF-β1/Smad 3 signaling pathway-related proteins in cells of each group. RESULTS AND CONCLUSION:(1)CCK-8 assay results suggested that 100 μg/mL silica was the best mass concentration and time to stimulate MRC-5 cells for 48 hours.(2)Immunofluorescence staining results showed that the expression of α-smooth muscle actin and collagen type I in the silica + human placental mesenchymal stem cell group was significantly lower than that in the silica group.(3)Western blot assay results showed that compared with the silica group,the protein expression levels of α-smooth muscle actin,collagen type I,N-cadherin,fibronectin,transforming growth factor-β1,p-Smad3,and Smad3 in the silica + human placental mesenchymal stem cell group were decreased,and the expression of E-cadherin was increased.The difference was statistically significant(P<0.05).(4)The results showed that human placental mesenchymal stem cells had a significant therapeutic effect on silica-induced pulmonary fibrosis.Human placental mesenchymal stem cells can inhibit the development of pulmonary fibrosis by regulating transforming growth factor-β1/Smad3 signaling pathway.