Fig. 3: Antifibrotic effects of the miR-150 secretome in an in vivo model of liver fibrosis.

a A schematic illustration showing the process of in vivo experiments. Mice with liver fibrosis were intravenously infused with normal saline (n = 12), the control secretome (n = 12), or the miR-150 secretome (n = 12) three times a week for 1 week. b RT-PCR results showing the mRNA expression of MMP2, α-SMA, and TGF-β1 in liver specimens in each group. The infusion of either the control or miR-150 secretome significantly reduced the mRNA expression levels of MMP-2, α-SMA, and TGF-β1 in the liver compared to those of infusion of normal saline, particularly in the mice with liver fibrosis. Comparing the two secretome groups, infusion of the miR-150 secretome induced significantly lower levels of MMP-2 and TGF-β1 expression in the liver specimens compared to those of infusion of the control secretome (P < 0.05). There was no significant difference in the expression of α-SMA between the two secretome groups. c Western blot analysis showing the effects of the miR-150 secretome on the expression of fibrosis-related markers in an in vivo model of liver fibrosis. Infusion of the miR-150 secretome induced higher expression of PCNA (a proliferation marker) and lower expression of fibrosis-related markers (α-SMA, TGF-β1, MMP-2, and TIMP-1) in the liver specimens compared with the levels obtained from infusion of the control secretome. The values are presented as the mean ± standard deviation of three independent experiments. *P < 0.05. α-SMA alpha-smooth muscle actin, Ct control, MMP-2 metalloproteinases-2, PCNA proliferating cell nuclear antigen, Sec the secretome obtained from ASCs after 48 h of incubation, TAA thioacetamide, TGF-β transforming growth factor-β; TIMP-1 tissue inhibitor of metalloproteinases-1, t-Sec the secretome released from miR-150-transfected ASCs.