Recent studies suggest that glial cells play an impor-tant role in nervous system. Like astrocytes in the central nervous system,satellite glial cells( SGCs) also participate in the physio-logical and pathological processes of the peripheral nervous sys-tem. SGCs affect neuronal functions through neuro-glial interac-tions. In this review,we summarize the current understanding of how SGCs affect the function of neurons.

Objective:To study the cytotoxic effects on three glioma cell lines U343, U138, U373 induced by anti-human DR5/DR4 monoclonal antibodies(FMU1.5/FMU1.4) and the underlying mechanism.Methods:Expression of DR4/DR5 was quantitated by flow cytometry and DR/4DR5 mRNA detected by RT-PCR. Cytotoxicity exerted by FMU1.4/FMU1.5 on three cell lines was measured by MTT colorimetry and the induced apoptosis was determined by agarose gel electrophoresis, DNA ploidy analysis was studied by flow cytometry.Results:The expression of DR5 on U343 cells was higher and the expression of DR4 on U373 cells was lower. Cell line U343 was sensitive to FMU1.5 and in a dose dependent manner, but it was partially sensitive to FMU1.4; Cell line U138 was partially sensitive to FMU1.5 and resistant to FMU1.4; Cell line U373 was insensitive to two antibodies.Conclusion:Apoptosis induced by monoclonal antibodie FMU1.4/FMU1.5 vary among three cell lines. The underlying mechanism may be relevant to DR4/DR5 expression,the release of cytochrome C and FLIP.

The mRNA expression levels of resistin in omental and abdominal subcutaneous adipose tissues were measured by one-step semi-quantitative RT-PCR in normal controls and metablic syndrome patients with or without type 2 diabetes. The results suggest that there is no relationship between resistin mRNA expression in omental and abdominal subcutaneous adipose tissue and metablic syndrome.

Objective To explore the effect of vitamin K2 on β-glycerophosphate(β-GP)-induced rat vascular smooth muscle cells (VSMCs) calcification and and the mechanism.Methods VSMCs were obtained from rat aortic,and identified by immunocytochemistry,then randomly divided into control group,high phosphorus group,vitamin K2 group (the group was settled three subgroups according to the concentration of vitamin K2 based on the high phosphorus medium,namely 10 μmol/L,25 μmol/L,50 μmol/L) and noggin (bone morphogenetic protein pathway inhibitor) group.Calcification was visualized by Alizarin red staining,calcium load in cells was quantified by o-cresolphthalein complexone method and alkaline phosphatase (ALP) activity was measured after stimulating 14 days,gene expressions of bone morphogenetic protein-2 (BMP-2),SMAD1,SMAD7 and Runx2 mRNA were detected by RT-PCR,Runx2 protein levels was detected by Western blotting after stimulating 3 days.Results Compared with the cells in control group,high phosphorus induced cell calcification,increased ALP activity,up-regulated the expression of BMP-2,SMAD1,Runx2 mRNA (P ＜ 0.05) and down-regulated the expression of SMAD7 (P ＜ 0.01),while compared with high phosphorus group,the calcium deposition,ALP activity and the expression of BMP-2,SMAD1,Runx2 mRNA were remarkably reduced in a dose-dependent manner by treatment with vitamin K2 (P ＜ 0.05) and the expression of SMAD7 was increased (P ＜ 0.01).Compared with high phosphorus group,SMAD1 and Runx2 expression in noggin group were remarkably reduced(P ＜ 0.01).Conclusion Vitamin K2 inhibits β-glycerophosphate-induced VSMCs calcification which correlates with the suppression of the expression of osteoblast markers through the down-regulation of bone morphogenetic protein pathway.

Objective:To detect the effect of EphrinA1-Fc on the phosphorylation of EphA2 and extracellular signal-regulated ki-nase (ERK) in 786-O renal carcinoma cells (RCCs). Methods:The soluble ligand EphrinA1-Fc was used to inhibit the 786-O RCCs in vitro. Western blot analysis was used to examine the phosphorylation of EphA2 and ERK1/2 in the 786-O RCCs at different time points. Results:After the intervention with EphrinA1-Fc for 5, 10, 30, and 60 min, the expression of p-EphA2 increased (F=9.392, P=0.025) as well as that of p-ERK (F=4.428, P=0.041). No p-EphA2 and p-ERK expression was observed in the pre-intervention group. Conclusion:One of the possible mechanisms of the inhibitory effect of EphrinA1-Fc on tumor metastasis and recurrence involves the phosphorylation of EphA2 by EphrinA1-Fc, leading to the degradation of EphA2.

Objective To explore the effect and mechanism of magnesium on calcification induced by hyperphosphate.Methods Vascular smooth muscle cells (VSMCs) were primarily cultured in vitro and induced calcification by β-glycerophosphate (β-GP).VSMCs were randomly divided into control group,high phosphorus group (10 mmol/L β-GP),magnesium intervèntion group(10 mmol/L β-GP + 3 mmol/L MgSO4) and 2-aminoethoxy-diphenylborate (2-APB,an inhibitor of magnesium transporter) intervention group(10 mmol/L β-GP+3 mmol/L MgSO4+ 10-4 mol/L 2-APB).Calcium deposition and alkaline phosphatase (ALP) activity were measured by alizarin red staining,quantification of calcium and euzyme linked immunosorbent assay.RT-PCR and Western blotting were used to observe the expression of core binding factor α-1 (Cbfα-1) mRNA and protein,respectively.In vivo,male Sprague-Dawley rats (n=24) were randomly divided into control group (methylcellulose+high phosphorous diet),vascular calcification group (adenine suspension + high phosphorous diet),high magnesium intervention group(adenine suspension+high phosphorous and magnesium diet).The aortic pulse wave velocity (PWV) was measured,and vascular calcification was determined by von Kossa stain and quantification of calcium.Cbfα-1 in aortic was measured by immunohistochemistry.Results In vitro,compared with high phosphorus group,calcification,ALP activity (P ＜ 0.05) and Cbfα-1expression in VSMCs were significantly decreased in magnesium intervention group after incubation for 14 days,but the addition of 2-APB might inhibit the protective effect of magnesium on VSMCs.Dynamic observation of Cbfα-1 showed that magnesium significantly inhibited the expression of Cbfα-1 (P ＜ 0.05) on the third day and the inhibitory role was obviously increased in a time-dependent manner.Consistent with the findings in vitro,the aortic PWV,calcification were all significantly reduced (P ＜ 0.05) in high magnesium intervention group with high serum magnesium level,when compared with vascular calcification group.Immunohistochemistry showed that hypermagnesemia downregulated obviously the expression of Cbfα-1 induced by hyperphosphatemia(P ＜ 0.05).Conclusion Magnesium protects against vascular calcification by inhibiting osteogenic differentiation of VSMCs.

Objective To investigate the relationship between polymorphisms in mitochondrial displacement-loop (mtDNA D-loop) and renal cell carcinoma. Methods Fifty-nine patients with clear cell renal cell cancer (renal cancer group) and 68 healthy control (control group) were selected in this study. The mtDNA D-loop region was amplified and se-quenced using polymerase chain reaction (PCR). Data were compared and analysed with the Revised Cambridge Reference Sequence (rCRS) in library of mitochondria. The difference in frequency analyses of mtDNA D-loop region was compared be-tween two groups. Results A total of 143 single nucleotide polymorphisms (SNP) of mitochondria D-Loop region were de-tected in renal cancer group and control group. Compared with control group, there were significantly higher frequencies of 262T and 16293G alleles in mitochondria D-loop region, and significantly lower frequencies of 16298C and 16319A alleles, in renal cancer group (P<0.05). Conclusion The analysis of genetic polymorphisms in the D-loop can be used as predic-tors of renal cell carcinoma and contribute to the early detection in patients of renal cell carcinoma.

Objective To explore the effects of the different concentrations of magnesium ions on vascular smooth muscle cell (VSMC) calcification in rats. Methods VSMCs were obtained from rat aortic, and were identified by immunocy-tochemistry. VSMCs were then randomly divided into control group, high phosphorus group and magnesium intervention group. VSMCs were cultured with 10%fetal bovine serum in control group. VSMCs were cultured with high phosphorus in high phosphorus group. VSMCs were cultured with different concentrations of magnesium chloride based on the high phos-phorus medium in magnesium intervention group (final concentrations of magnesium ions were 1, 2 and 3 mmol/L). The calci-um content and alkaline phosphatase(ALP)activity were measured after the stimulation for 7 days. The expression of Cbfα1 mRNA was detected by RT-PCR. Results Compared with control group, calcium deposits were found significantly higher in high phosphorus group and magnesium intervention group. The calcified nodules gradually reduced with the increased magnesium ion concentration in the intervention group. The calcium contents were significantly lower in the intervention groups (2 and 3 mmol/L) compared with those of high phosphorus group (P<0.05), but no difference was found between 1 mmol/L magnesium intervention group and high phosphorus group. There were no significant differences in the ALP activity and Cbfα1 mRNA expression between intervention groups (2 and 3 mmol/L) and control group (P<0.05). The ALP activity and the expression of Cbfα1 mRNA were gradually decreased with the increased magnesium ion concentration in the inter-vention group, and which were lower than those of high phosphorus group (P<0.05). Conclusion Magnesium can reduce calcification and osteoblastic transdifferentiation, which may be achieved by reducing the expression of Cbfα1 in VSMCs.

Objective To explore the effect of different pH values on calcification of rat vascular smooth muscle cells (VSMCs) through bone morphogenetic protein (BMP)-2 signaling pathway. Methods Healthy male SD rats aged 5-8 weeks were selected in the study. VSMCs from rat thoracic aorta were cultured in vitro, and then identified by immunocytochemistry. The VSMCs were randomly divided into 4 groups by random sampling method:normal group (pH 7.4), pH7.4+high phosphorus group, pH 7.1+high phosphorus group, and pH 7.7+high phosphorus group. Calcium deposition and alkaline phosphatase (AKP) activity were measured by alizarin red staining and enzyme linked immunosorbent assay. The expressions of BMP-2, Smad1 and Runx2 mRNA were detected by RT-PCR. Results Compared with the control group, the calcification staining was increased in pH 7.4+high phosphorus group, calcium content was increased and expressions of BMP-2, Smad1, Runx2 mRNA and AKP activity were also increased (P<0.05). While compared with the pH 7.4+high phosphorus group, calcification staining, calcium content, expressions of BMP-2, Smad1, Runx2 mRNA and AKP activity were decreased in pH 7.1+high phosphorus group (P<0.05). The calcification staining, calcium content, expressions of BMP-2, Smad1, Runx2 mRNA and AKP activity were increased in pH 7.7+high phosphorus group (P<0.05). Conclusion The extracellular acidic environment (pH 7.1) can inhibit high-phosphotus-induced VSMCs calcification, whereas extracellular alkaline environment (pH 7.7) induce high-phosphotus-induced VSMCs calcification. The mechanism is presumably that VSMCs calcification is induced by influencing BMP-2 pathway, which may be mediated by VSMCs phenotype transdifferentiation of BMP-2 signaling pathway.

Objective:To study the effects of Anti-DR5 mAb on inducing synovial cells of adjuvant arthritis (AA) rats and its mechanisms.Methods:AA was induced by CFA in rats.The synovial cells of rats were separated and cultured in vitro system.The apoptosis induced by anti-DR5 mAb on synovial cells was measured by MTT analysis,DNA fragmentation and flow cytometry.Caspase-3 and Bcl-2 expression in synovial cells were detected by Western blot.The involvement of the apoptotic pathway was further proved by a caspase inhibition assay.Results:MTT result showed that Anti-DR5 mAb could inhibit synovial cells growth.And flow cytometry suggested that the cell death mode was apoptosis.The protein level of caspase-3 in synovial cells treated with anti-DR5 mAb was raised,while Bcl-2 level declined.When the caspase inhibitor was added to the synovial cells treated with anti-DR5 mAb,it was showed in a dose-dependence inhibition effect,indicating that anti-DR5 mAb inducing apoptosis might be through the caspase pathway.Conclusion:Anti-DR5 mAb could induce synovial cell apoptosis through caspase pathway.And this effect may be related to the protein level of Caspase-3 and Bcl-2.