Neovascularization has a critical role in the growth and metastatic spread of tumors, and involves recruitment of circulating endothelial progenitor cells (EPCs) from bone marrow. In this study, we examined whether EPCs could promote tumor angiogenesis, and found that the tumor growth was enhanced by the administration of EPCs. To test the hypothesis that genetically modified bone marrow-derived EPCs can be effective carriers of therapeutic agents to tumor sites, we conducted human interferon-beta (HuIFN-b) gene transfection of EPCs with a virus vector in vitro. When HuIFN-b was applied in the ex vivo culture of EPCs, HuIFN-b-transduced EPCs achieved efficient killing of the total population of SPC-A1 cells, indicating a bystander effect was elicited by HuIFN-b-transduced EPCs in vitro. When SCP-A1 cancer cells were coimplanted along with ex vivo cultivated EPCs subcutaneous injection in nude mice, the tumor growth was increased. However, the anti-tumor effect of interferon-beta (IFN-b) offset the tumor-progressive character of EPCs and the tumor growth, and the vascular density of tumor tissues increased by coimplanted EPCs were decreased upon IFN-b treatment. In addition, overall expression levels of vascular endothelial growth factor in tumor tissues were decreased upon IFN-b treatment. Therefore, our results suggest that gene-transfected EPCs could be useful as a tumor-specific drug delivery system.
The elastic free energy of carbon nanotubes grown by iron-catalyzed decomposition of acetylene is introduced to describe the possible tubular shapes. The equilibrium shape equation can be obtained by the first variation of the elastic free energy of the slightly distorted tube. The model is consistent with both stable and metastable shapes observed in our experiments. The results are due to the fluctuation of growth conditions, such as the pressure, temperature, and composition of the vapor.
Background The life time risk of developing heart failure is 20% for Americans over 40 years old. Chronic heart failure (CHF) is becoming a global health problem in the elderly. Previous studies indicate that immune-inflammatory activation plays an important role in the pathogenesis of myocardial fibrosis in CHF. Paeoniflorin (PF) is one of the main effective components of peony, which has been widely used in traditional Chinese medicine for its potent immunomodulatory and anti-inflammatory properties. However, the effects of PF on myocardial fibrosis remain unclear. Objective To exam whether PF protects myocardial fibrosis and improves cardiac function in isoprenaline-induced CHF rats. Methods Age matched male Wistar rats were used in this study. CHF and cardiac remodelling model was established by hypodermic injection of isoprenaline for ten days. After the CHF model establishment, the rats were randomly divided to receive placebo, PF (50 or 100 mg/kg/d, i.g.) or captopril for six weeks. Cardiac remodelling markers including ventricular mass, collagen volume fraction, perivascular collagen area and hydroxyproline concentration were studied. Echocardiography, Masson staining, immunohistochemistry, western blot and real-time PCR were performed. The protein and mRNA expression of PTEN (phosphatase and tensin homolog deleted on chromosome ten) were analysed. Results Compared to the untreated CHF rats, the perivascular collagen area, collagen volume fraction (30.97 ± 4.22% vs 13.75 ± 3.77%), hydroxyproline concentration (4.92 ± 0.78 μg/mg wet weight vs 2.08 ± 0.43 μg/mg wet weight), LVIDd (8.40 ± 0.52 mm vs 6.11 ± 0.58 mm) and LVIDs (6.44 ± 0.93 mm vs 4.49 ± 0.38 mm) were significantly lower in PF-treated (100 mg/kg/d) rats (p < 0.05, n = 8). PF treatment also improved LVEF levels (46.44 ± 3.50% vs 60.89 ± 3.10%). Besides, the expressions of PTEN protein (0.11 ± 0.05 vs 0.63 ± 0.19, p < 0.05) and mRNA (0.22 ± 0.06 vs 0.39 ± 0.02, p < 0.01) were higher in PF-treated rats (n = 3). No damage of renal or liver function was detected in these rats (p > 0.05). Furthermore, we also found that PF can accelerate myocardial fibroblast cell apoptosis and upregulate PTEN signalling in vitro . Conclusions Our findings indicate that PF could alleviate myocardial fibrosis and improve cardiac function in isoprenaline-induced CHF rats by upregulating PTEN signalling pathway. PF may be a potential therapeutic drug for CHF.
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