Objective To investigate the immunologic properties of osteogenic differentiated bone mesenchymal stem cells (BMSCs). Methods BMSCs were isolated from normal volunteers and induced in osteogenic medium for two weeks. Then,non-differentiated/osteogenic differentiated BMSCs were co-cultured with allogenic T cells and phytohemagglutinin (PHA).The proliferation of T cells was examined by MTT method.The concentrations of TGF-β1 in osteogenic differentiated BMSCs supernatants at week 2 and mixed lymphocytes reaction (MLR) supernatants at day 5 were determined by ELISA.Also,anti-TGF-β antibody was added into the MLR to detect the response of the mixed T cells. Results Non-differentiated and osteogenic differentiated BMSCs did not induce proliferation of the allogeneic T cells but both suppressed the proliferation of the T cells mediated by PHA.The TGF-β1 concentrations had significant elevation in the MLR.Anti-TGF-β antibody could counteract the immunosuppressive function of the osteogenic differentiated BMSCs. Conclusion Osteogenic differentiated BMSCs possess low immunogenicity and immunosuppressive property.

BACKGROUND:Related studies have shown that after kyphoplasty with bone cement injection, the vertebral height restoration is closely related to the injury time. Surgical timing also has an important influence on the incidence of postoperative complications. OBJECTIVE:To compare the clinical efficacy of kyphoplasty with bone cement injection at 2 and 2-4 weeks after thoracolumbar vertebral compression fractures, and to investigate the best timing for kyphoplasty. METHODS:Eighty-two thoracolumbar fracture patients, aged 55-85 years old, were included. Thirty-nine cases were subjected to kyphoplasty with bone cement injection within 2 weeks after injury. Another 43 cases were subjected to kyphoplasty with bone cement injection within 2-4 weeks after injury. The visual analog scale score, restoration of anterior and central vertebral height, volume and leakage of bone cement after treatment were compared between two groups. At 6 months after treatment, the daily activities of patients in the two groups were evaluated using Oswestry disability index. RESULTS AND CONCLUSION:Immediately and at the 6th month after treatment, the scores on the visual analog scale and the Oswestry disability index were lower than those before treatment (P < 0.05). The visual analog scale score immediately after treatment in the treatment group within 2 weeks was higher than that in the treatment group within 2-4 weeks (P< 0.05). After 6 months of treatment, there was no significant difference in the restoration rate of anterior and central vertebral height between these two groups, but the loss rate of the anterior and central vertebral height in the treatment group within 2 weeks was lower than that in the treatment group within 2-4 weeks (P< 0.05). Bone cement injection volume and leakage rate had no significant differences between two groups. These results demonstrate that patients appeared to have obvious pain after percutaneous kyphoplasty with bone cement injection within 2 weeks, but the percutaneous kyphoplasty with bone cement injection had smal influence on the short-term loss rate of vertebral height. Therefore, percutaneous kyphoplasty with bone cement injection with 2 weeks after injury is the optimal treatment timing for patients with thoracolumbar compression fractures.

BACKGROUND:Fractures can induce bone cel hypoxia, and remarkably reduce the oxygen tension in cels. Hypoxia-inducible factor-2α is a key oxygen-dependent transcriptional activator to regulate the body function under hypoxia and mediate the release of various inflammatory factors after fractures.
OBJECTIVE:To explore the role of Laquinimod in expression and function of hypoxia-inducible factor-2αin osteoblasts.
METHODS: Mouse osteoblasts MC3T3-E1 (clone 14) were pretreated with Laquinimod at various concentrations(10-100μmol/L) before hypoxia in the presence or absence of specific proteasome inhibitors MG132 or N-acetyl-leucyl-leucyl-norleucine. Then, the media were pre-conditioned in 1% or 21% oxygen tension for 1 to 24 hours.
RESULTS AND CONCLUSION: Under hypoxia, the expression of hypoxia-inducible factor-2α in osteoblasts was increased remarkably, and Laquinimod could inhibit the expression of hypoxia-inducible factor-2α and its target genes in mouse MC3T3-E1 cels. Mechanisticaly, Laquinimod promoted hypoxia-inducible factor-2α degradation in a proteasome-dependent but von Hippel-Lindau protein-independent manner. Importantly, we found that Laquinimod disrupted the interaction between hypoxia-inducible factor-2α and its chaperone heat shock protein 90, but promoted the interaction between hypoxia-inducible factor-2α and the receptor of activated protein kinase C. These findings suggest that Laquinimod may promote the degradation of hypoxia-inducible factor-2α by affecting its folding and maturation. Laquinimod is a novel inhibitor of hypoxia-inducible factor-2α by changing its functional interaction with chaperone proteins heat shock protein 90 and receptor of activated protein kinase C.