Bone mesenchymal stem cells (BMSCs) have been an area of interest in biomedical research and tissue engineering due to their diverse differentiation abilities. In osteogenesis, bone morphogenetic proteins (BMPs), particularly BMP-2, are important. However, the effect of BMP-2 on the osteogenetic capacity of BMSCs remains to be fully elucidated. In the present study, primary rat BMSCs were infected with a recombinant lentivirus carrying the BMP-2 gene (Lenti-BMP-2), and the effects of BMP-2 on the activity of alkaline phosphatase (ALP) on days 3, 7, 14 and 21, and on mineralization on day 21 were evaluated. In addition, the adhesive ability of BMP-2-overexpressed BMSCs was detected using an adhesion assay. Following forced expression of BMP-2 in the BMSCs, the levels of osteogenic genes, including osteopontin (OPN), osteocalcin (OC) and collagen type I (Col-I), were detected and the nuclear accumulation of Runt-related transcription factor (Runx)-2 and phosphorylated small mothers against decapentaplegic (p-Smad) 1/5/8 was also evaluated. The results demonstrated that the rat BMSCs had been isolated, cultured and passaged from Sprague-Dawley rat bone marrow successfully, and the third-generation BMSCs were identified using flow cytometry with CD29 staining. The osteogenetic phenotype of the BMSCs, expressing ALP and osteocalcin, was significantly induced by BMP-2, and the proliferation of the BMSCs was enhanced by BMP-2. Furthermore, the adhesive potential of the BMP-2-overexpressed BMSCs was increased, the expression levels of OPN, OCN and Col-Ie osteogenetic factors were upregulated and the nuclear accumulation of Runx-2 and p-Smads1/5/8 were increased significantly. These data suggested that BMP-2 may facilitate the osteogenetic differentiation of rat BMSCs and provide a favorable cell resource for tissue engineering.

Understanding the role and underlying regulation mechanism of autophagy in lipopolysaccharide-induced lung injury (LPS-LI) may provide potentially new pharmacological targets for treatment of acute lung injury. The aim of this study was to investigate the functional significance of autophagy in LPS-LI. The autophagy of human pulmonary microvascular endothelial cells (HPMVECs) and mice was inhibited before they were challenged with LPS. In vitro, permeability, vitality, and the LDH release rate of the cells were detected, the zonula occluden-1 (ZO-1) expression and the stress fiber formation were determined. In vivo, the lung injury was assessed. We found LPS caused high permeability and increased lactate

No abstract