Aberrantly expressed miR-155 is associated with renal rejection after allogeneic transplantation. This study mainly explored the mechanism of miR-155 derived from bone marrow mesenchymal stem cell-secreted exosomes (BMSC-exo) in renal rejection after allogeneic transplantation. Thirty Fischer rats and 40 Lewis rats were used as donors and recipients, respectively. The Lewis rats were randomized into 4 groups (10 rats per group): Control group, miR-155 group, positive control group and CXCR4 agonist group. The following indicators were monitored in BMSC-exo: miR-155 expression, serum creatinine level, renal histopathological changes, CADI score, number of cells that were positive for TGF-β, Smad3 and α-SMA, as well as the protein levels of Smad3, TGF-β, CXCR4 and SDF-1. miR-155 expression in BMSC-exo was significantly higher than that in HKb-20 cells. On the 7th day after surgery, the serum creatinine levels of rats in the miR-155 group and positive control group reduced significantly, while decreasing slowly in the control group and CXCR4 agonist group. The CADI scores of rats in the miR-155 group and positive control group were significantly higher than those in the control group and CXCR4 agonist group (P < 0.05). No significant difference was found either between the miR-155 group and positive control group, or between the control group and CXCR4 agonist group (P > 0.05). Rats in the control group and CXCR4 agonist group had more cells that were positive for TGF-β, Smad3 and α-SMA, while those in the miR-155 group and positive control group showed less. The Smad3, TGF-β, CXCR4 and SDF-1 proteins were weakly expressed in the miR-155 group and positive control group, but strongly expressed in the control group and CXCR4 agonist group. No significant difference in the protein levels was found either between the miR-155 group and positive control group, or between the control group and CXCR4 agonist group (P > 0.05). miR-155 derived from BMSC-exo is protective against allogeneic kidney transplantation. Specifically, BMSC-exo-derived miR-155 blocked the activity of SDF-1/CXCR4 and TGF-β/Smad3 pathways, thereby downregulating the expression of α-SMA. As a result, it ameliorated renal fibrosis and alleviated renal dysfunction, ultimately leading to the prevention and reduction of renal rejection following allograft transplantation.

Bone marrow-derived mesenchymal stem cells (BMSCs) are an integral part of the tumor microenvironment and involved in tumor evolution. Our aim is to further illuminate the relationship of exosomes of BMSC origin and breast cancer cells in breast cancer. Differential diagnosis was performed by identifying exosomal miR-206 secreted by BMSCs, and RT-PCR detected miR-206 expression in tumor tissues. Transwell assayed cell function and Target scan analyzed the regulatory relationship between Rab23 and miR-206. Rab23 expression was examined by western-blot after the addition of Rab23 and the effect of Rab23 on hedgehog was further verified. We demonstrated that exosomal miR-206 from BMSCs is expressed in tumor tissues and miR-206 mimics significantly inhibited tumor cell invasion and proliferation. miR-206 targets Rab23 and negatively regulates its expression. Further results showed that the addition of Rab23 could activate hedgehog signaling and promote the development of breast cancer. In conclusion, our study reveals that BMSC-derived miR-206 activates hedgehog gene signaling and promotes the breast carcinogenesis development by regulating Rab23 expression.