ObjectiveTo investigate the role of myeloid-derived suppressor cell (MDSC) in bleomycin (BLM)-induced pulmonary fibrosis and the possible mechanism of bone marrow mesenchymal stem cell (MSC) in therapy of BLM-induced pulmonary fibrosis.MethodsBone marrow mesenchymal stem cells (MSC) were harvested from 6-week old male BALB/c mice. One hundred and four female BALB/c mice were randomly divided into 3 groups. Mice in control (n=32) and BLM group were instilled with normal saline (NS) or BLM via trachea and NS were injected via tail vein on the 1st, 2nd and 3rd day after NS administration. Mice in MSC group (n=40) were instilled with BLM via trachea and MSC (total cell number=1.5×106) were injected via tail vein. On the 1st, 3rd, 5th, 8th, 11th, 14th, 18th, 21st, 25th and 32nd day after BLM administration, the percentage of Gr-1+CD11b+ cells in peripheral blood mononuclear cell (PBMC) was detected by flow cytometry. Eight mice from each group were killed on the 3rd, 8th, 18th and 32nd day after BLM administration, the percentage of Gr-1+CD11b+ cells in the lung tissue was detected by flow cytometry. Meanwhile, the lung tissue specimens were stained with Masson. The sry gene of Y chromosome was detected by polymerase chain reaction (PCR).ResultsCompared with BLM group, MSC transplantation significantly reduced pulmonary inflammation in MSC group [(1.32±0.25) vs. (2.53±0.56); and (1.06±0.42) vs. (2.27±0.82), respectively, P<0.01)]. Likewise, MSC transplantation significantly reduced pulmonary fibrosis and deposition of collagen as compared with BLM group [(1.02±0.44) vs. (1.81±0.74), and (1.51±0.73) vs. (2.72±0.54), respectively, P<0.05)]. The percentage of Gr-1+CD11b+ cells in the BLM group was significantly increased as compared with control group. Compared with BLM group, MSC transplantation significantly reduced Gr-1+CD11b+ cells in MSC group (P<0.05). The sry gene (201 bp) was detected in the lungs of female mice within 96 hours after MSC administration.ConclusionsMDSC participates in the procedure of BLM-induced pulmonary fibrosis. Syngeneic MSC inhibits the generation of MDSC and further suppresses BLM-induced pulmonary fibrosis.
ObjectiveTo summarize the possible roles and relevant mechanisms of solute carrier family 3 member A2 (SLC3A2) gene in hepatocellular carcinoma (HCC), and explore its clinical application prospects and value in the diagnosis, treatment, and prognosis of patients with HCC. MethodThe literature on reseaches of the SLC3A2 gene and its association with HCC both domestically and internationally in recent years was reviewed and summarized. ResultsNotably, the SLC3A2 exhibited obviously elevated expression in the HCC tissue as compared with the normal liver tissue. It mainly affected the disease progression of HCC by regulating the intracellular and extracellular amino acids transport, inhibiting the ferroptosis of cells, activating the mechanistic target of rapamycin complex signaling pathways and integrin signaling pathway, and played an important role in the diagnosis, treatment, and prognosis of patients with HCC. ConclusionFrom the results of literature review collected, SLC3A2 might be closely associated with the migration, invasion, proliferation, and apoptosis of HCC cell, and it is expected to serve as an indicator for evaluating survival and prognosis of patients with HCC, and become one of the effective treatment targets for HCC in future.