Negative pressure promotes epidermal differentiation of bone marrow mesenchymal stem cells / 中国组织工程研究

BACKGROUND: As a physical factor, negative pressure can promote the osteogenic differentiation and endothelial differentiation of mesenchymal stem cells. If a negative pressure exerts effects on the epidermal differentiation of mesenchymal stem cells, it will be highly important for the combination use of negative pressure and mesenchymal stem cells in wound healing. OBJECTIVE: To explore the effect of negative pressure on the epidermal differentiation of bone marrow mesenchymal stem cells. METHODS: Bone marrow mesenchymal stem cells of New Zealand white rabbits were isolated and cultured. Then, the passage 3 cells were induced for epidermal differentiation under negative pressure (-16.625 kPA, twice a day, once for 4 hours) as experimental group. Another cells induced under no negative pressure were used as control group. After induction, cell growth curve was drawn in each group, and the expression of cytokeratin 5 and cytokeratin 10 mRNA was examined by real-time PCR at 2 weeks after induction. RESULTS AND CONCLUSION: The cell growth of the experimental group was inhibited, and the mRNA expression of cytokeratin 5 and cytokeratin 10 was significantly increased compared with the control group (P < 0.05). These findings indicate that under the condition of negative pressures, the epidermal differentiation ability of bone marrow mesenchymal stem cells is increased, and in contrary, the cell proliferation is inhibited.

Effect of shRNAmir lentiviral vector-mediated COX-2 silencing on the radiosensitivity of nasopharyngeal carcinoma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the effect of COX-2 silencing on the radiosensitivity of a nasopharyngeal carcinoma (NPC) cell line C666-1.</p><p><b>METHODS</b>Anti-COX-2 C666-1 cell line with COX-2 gene silencing mediated by shRNAmir lentiviral vector and the control cell line Anti-GL-2 C666-1 were exposed to various radiation doses. The clonogenic survival assay and curve fitting was used to calculate the radiobiological parameters and the sensitization enhancement ratio after the radiation. Cell cycle changes were assessed after the exposure by flow cytometric analysis. In a BALB/c nude mouse model, the growth curve of the xenografts was generated and the tumor growth inhibition rate was calculated.</p><p><b>RESULTS</b>Compared with the control cells, Anti-COX-2 C666-1 cells showed obviously lowered values of SF2, D0 and Dq but significantly increased α/β with a sensitivity enhancement ratio of 1.4014. COX-2 gene silencing increased the inhibition rate of the tumor xenografts after the radiation, and caused also decreased percentage of G2/M arrest resulting from the exposure.</p><p><b>CONCLUSION</b>Stable COX-2 silencing in NPC cells can improve the effect of radiotherapy both in vitro and in vivo. By changing the radiobiological parameters, genetically based COX-2 inhibitor may be a potentially promising radiosensitizer of NPC.</p>

Pericyst may be a new pharmacological and therapeutic target for hydatid disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Most hydatid cysts with calcified walls are biologically and clinically silent and inactive. Transforming growth factor-beta 1 (TGF-β1) plays a critical role in the calcification process of cells. The aim of this study was to assess the effect of modulating TGF-β1 signaling on the calcification of hydatid cysts.</p><p><b>METHODS</b>Pericyst cells isolated from hepatic hydatid cysts were cultured with osteogenic media. These cells were assessed for alkaline phosphatase activity and mineralization capacity using Alizarin Red staining. Cells were also treated with recombinant human TGF-β1 and TGF-β inhibitor, and the expression profiles of osteoblast markers (RUNX2, osterix, and osteocalcin) were analyzed using Western blotting. The effects of inhibiting TGF-β1 signaling on calcification of pericyst walls were assessed using different doses of TGF-β inhibitor for 7 weeks in a preclinical disease model of liver cystic echinococcosis.</p><p><b>RESULTS</b>Cells within the pericyst displayed high levels of alkaline phosphatase activity and mineralized nodule formation, as induced by osteogenic media. These activities, as well as expression profiles of osteoblast markers (RUNX2, osterix, and osteocalcin) could be inhibited by addition of recombinant human TGF-β1 (rhTGF-β1) and enhanced by TGF-β inhibitor. In the animal model of cystic echinococcosis, inhibition of TGF-β1 signaling increased calcification of the pericyst wall, which was associated with decreased cyst load index and lower viability of protoscoleces.</p><p><b>CONCLUSIONS</b>Cells within the pericysts adopt an osteoblast-like phenotype and have osteogenic potential. Inhibition of TGF-β1 signaling increases hydatid cyst calcification. Pharmacological modulation of calcification in pericysts may be a new therapeutic target in the treatment of hydatid disease.</p>