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The effects of transplanting bone marrow mesenchymal stromal cells (BMSCs) for the treatment of white matter damage are not well understood, nor are the underlying mechanisms. Recent studies showed that endogenous oligodendrocyte progenitor cells (OPCs) can be stimulated to proliferate. Therefore, we explore the effects of BMSCs transplantation on white matter damage and the proliferation of OPCs in transient focal cerebral ischemic rats. BMSCs were transplanted into a group of rats that had undergone middle cerebral artery occlusion (MCAO) 24 h after reperfusion. The ratswere examined by MRI-T2 and DTI sequencesdynamically. The proliferating cells were labeled by 5-Bromo-2'-deoxyuridine (BrdU). The effects of BMSC transplantation on neurons, axons, myelination, and proliferating OPCs were examined by Nissl staining, MBP/NF-H and BrdU/NG2 immunofluorescence staining7 days after transplantation. More Nissl-stained neuronswere found and the FA value of MRI-DTI was significantly higher in the MCAO + BMSCs group than in the MCAOgroup (both P < .01). The fold change of MBP protein was significantly higher in the MCAO + BMSCs group than in the MCAO group (P < .01); the same was true of NF-H protein. Additionally, there were more BrdU + NG2 + cells in the SVZ areas of the MCAO + BMSCs group than in the MCAO group (P < .01). BMSCs thus were shown to alleviate neuronal/axonal injury and promote the proliferation of OPCs and formation of myelin sheath, significantly alleviating white matter damage in focal cerebral ischemic rats., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background: microRNAs (miRNAs) have been verified as molecular targets for regulating tumor proliferation, invasion, and metastasis in tumor progression. However, the relationship between miRNAs and cellular energy metabolism in breast cancer still needs to be clarified. This study aimed to investigate the role of miR‐429 in breast cancer progression. Methods: Bioinformatic analyses were employed to detect the relationship between miR‐429 and cancer‐related signaling pathways. We used a Kaplan‐Meier curve to analyze survival rate in patients with high or low expression of miR‐429. We used real‐time quantitative PCR (RT‐qPCR) to detect the expression of miR‐429 in different cell lines. Sh‐con, over‐miR‐429, miR‐429 inhibitor, and sh‐inhibitor control were transfected. Colony formation and EDU assay were used to detect the proliferation of transfected cells. Wound healing and transwell assays were performed to detect the mobility and invasion ability of transfected cells. Western blot assay was used to detect relative protein expression in transfected cells and different tissues. Bioinformatic analyses were conducted to detect the target proteins expression in different breast cancer databases. Dual luciferase reporter assay was used to confirm the binding site between miR‐429 and fibronectin 1 (FN1). Results: The results of our study indicate that MiR‐429 and its target genes are associated with cancer‐related signaling pathways and that higher miR‐429 expression corresponds with a better prognosis. When miR‐429 was overexpressed, the proliferation, invasion of MDA‐MB‐231 were inhibited. MiR‐429 was able to suppress the Wnt/β‐catenin signaling pathway, and FN1 overexpression could rescue the influence of over‐miR‐429. Conclusions: The results of our study suggest that miR‐429 suppresses the proliferation and invasion of breast cancer via inhibiting the Wnt/β‐catenin signaling pathway. [ABSTRACT FROM AUTHOR]