Search

Liver fibrosis is a serious stage of chronic liver injury. Inhibition of hepatic stellate cells activation and hepatocytes apoptosis is important measures in the treatment of liver fibrosis. Studies have shown that exosomes are involved in regulating the information transmission between cells, but there are few studies on the interaction between exosomes from HSC and hepatocytes. This study screened miRNAs with significant differences related to liver fibrosis in the database. Then, we activated HSC applying transforming growth factor β1 (TGF-β1) and collected exosomes. The expression of miRNA in HSC-derived exosomes was verified by quantitative real-time PCR (qRT-PCR). The results of cell function test showed that HSC-derived exocrine miRNA-99a-5p could inhibit hepatocytes proliferation and promote hepatocytes apoptosis. Conversely, inhibition of miRNA-99a-5p can promote hepatocytes proliferation and inhibit apoptosis. Target gene prediction and luciferase assay show that miRNA can specifically bind to BMPR2 site sequence. In addition, we also detected the expression of BMPR2 and apoptosis-related protein by qRT-PCR and Western blot (WB). In conclusion, this study demonstrates that HSC-derived exocrine miRNA-99a-5p can promote hepatocytes apoptosis and participate in the process of liver fibrosis by targeting BMPR2. Our findings highlight the therapeutic potential of HSC-derived exocrine miRNA-99a-5p in hepatic fibrosis. [ABSTRACT FROM AUTHOR]

Forkhead box M1 (FoxM1), a proliferation specific transcriptional modulator, plays a principal role in many physiological and pathological processes. FoxM1-mediated oncogenic processes have been well addressed. However, functions of FoxM1 in immune cells are less summarized. The literatures about the expression of FoxM1 and its regulation on immune cells were searched on PubMed and Google Scholar. In this review, we provide an overview on the roles of FoxM1 in regulating functions of immune cells, including T cells, B cells, monocytes, macrophages, and dendritic cells, and discuss their contributions to diseases. [ABSTRACT FROM AUTHOR]