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Objective To explore the relationship between type 2 diabetes mellitus(T2DM)and serum stromal cell derived factor-1(SDF-1)levels. Methods A community-based epidemiological field study for T2DM patients and non-T2DM subjects was conducted in Beijing,China. Every subject underwent physical examinations, biochemical tests of stromal cell derived factor 1 and so on,and completed a standardized questionnaire. A total of 756 subjects were recruited in our analysis ,including 267 T2DM patients and 489 non-T2DM subjects ,T2DM patients were further divided into 81 simple T2DM patients and 186 macrovascular complication patients on the basis of the status of macrovascular complication. The correlation between serum SDF-1 levels and T2DM was analyzed. Results Compared with non-T2DM group,the level of SDF-1 in T2DM group was higher(P=0.019). The level of SDF-1 in simple T2DM group was also higher than macrovascular complication group(P=0.044). In the multi-ple linear regression analysis,after adjustment for age,gender,smoking,drinking,dyslipidemia,hypertension and BMI,SDF-1 level in simple T2DM group was higher than macrovascular complication group(P = 0.049), still. Conclusions Simple T2DM patients had a higher serum SDF-1 level than T2DM patients with macrovascular complications as well as those who did not suffer T2DM,suggesting that the stromal cell derived factor-1 may play a certain role in the development of T2DM and macrovascular complications.
ABSTRACT
Objective To explore the relationship between type 2 diabetes mellitus(T2DM)and serum stromal cell derived factor-1(SDF-1)levels. Methods A community-based epidemiological field study for T2DM patients and non-T2DM subjects was conducted in Beijing,China. Every subject underwent physical examinations, biochemical tests of stromal cell derived factor 1 and so on,and completed a standardized questionnaire. A total of 756 subjects were recruited in our analysis ,including 267 T2DM patients and 489 non-T2DM subjects ,T2DM patients were further divided into 81 simple T2DM patients and 186 macrovascular complication patients on the basis of the status of macrovascular complication. The correlation between serum SDF-1 levels and T2DM was analyzed. Results Compared with non-T2DM group,the level of SDF-1 in T2DM group was higher(P=0.019). The level of SDF-1 in simple T2DM group was also higher than macrovascular complication group(P=0.044). In the multi-ple linear regression analysis,after adjustment for age,gender,smoking,drinking,dyslipidemia,hypertension and BMI,SDF-1 level in simple T2DM group was higher than macrovascular complication group(P = 0.049), still. Conclusions Simple T2DM patients had a higher serum SDF-1 level than T2DM patients with macrovascular complications as well as those who did not suffer T2DM,suggesting that the stromal cell derived factor-1 may play a certain role in the development of T2DM and macrovascular complications.
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The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated.Concentration of maternal serum sFlt-1 protein was detected by ELISA.Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader.Morphologic change of ciGENC was observed under inverted phase contrast microscope.The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P＜0.01).Permeability in preeclampsia groups was significantly increased as compared with control group (P＜0.01).By contrast with severe preeclampsia group,the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P＜0.05).Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups.It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.
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It remains controversial whether tumor necrosis factor (TNF)-α antagonism is effective for asthma.This meta-analysis was performed to evaluate efficacy of TNF-α antagonism in treatment of patients with asthma.MEDLINE,EMBASE,LILACS,and CINAHL databases were searched for English-language studies published through January 3,2010.Randomized-controlled trials comparing TNF-α antagonism with control therapy were selected.For each report,data were extracted in relation to the outcomes analyzed:asthma exacerbation,asthma quality of life questionnaire scores,and forced expiratory volume in 1 second.Four assessable trials were identified including 641 patients with asthma.TNF-α antagonism therapy was superior to control therapy in preventing exacerbations in asthmatics [pooled odds ratio 0.52 (95％ confidence interval 0.29-0.88),P=0.02]; however,there was a nonsignificant reduction in asthma quality of life questionnaire scores [0.23 (0 to 0.47),P=0.05],forced expiratory volume in 1 second [0.03,(-0.14 to 0.10),P=0.74] when analyzed using standardized mean differences.TNF-α antagonism was superior to control chemotherapy in terms of asthma exacerbation,but not asthma quality of life questionnaire scores or forced expiratory volume in 1 second.
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This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerular disease in preeclampsia.SFlt-1 expression in the human trophoblasts (TEV-1 cells) was enhanced by transfecting sFlt-1 plasmid DNA into TEV-1 cells.The monolayer barrier function of glomerular endothelial cells (ciGEnCs) was determined by measuring the fluorescence intensity of bovine serum albumin (BSA) that crossed the monolayer of glomerular endothelial cells.The results showed that the over-expression of sFlt-1 by TEV-1 cells led to the barrier dysfunction of ciGEnCs,and the exogenous VEGF could alleviate the ciGEnCs dysfunction resulting from the over-expression of sFlt-1 to a certain extent.It was concluded that the dysregulation of sFlt-1 and VEGF in preeclamptic pregnancy may contribute to the barrier dysfunction of glomerular endothelial cells,and VEGF may play an important role in maintaining the barrier function of glomerular endothelial cells,but it may not be the sole factor.
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This study examined the association of expression of vascular endothelial growth factor(VEGF),a promoter of angiogenesis,with endothelium dysfunction in preeclampsia.The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry,real-time reverse transcriptase-polymerase chain reaction(RT-PCR)and enzyme-linked immunosorbent assay(ELISA),respectively.VEGF expression in the human umbilical vein endothelial cells(HUVECs)was blocked by small interfering RNAs(siRNAs).The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers.The cell proliferation and cell-secreted nitric oxide(NO)level were detected by MTT method and nitrate reductase assay,respectively.The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue.The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects,although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high.Moreover,VEGF deficit could lead to endothelium cell dysfunction,and the administration of VEGF could protect endothelium cells from injury.It was concluded that lack of VEGF contributes to endothelium dysfunction,which may lead to the occurrence and development of preeclampsia.
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In order to investigate the effect of Polo-like kinase-1 (Plk1) depletion on cell cycle pro- gression and cell growth in lung cancer cells, a recombinant plasmid containing antisense RNA tar- getting Plk1 (pcDNA3-Plk1) was transfected into A549 cells by lipofectine. RT-PCR and Western-blot were used to detect the Plk1 gene expression. Cell proliferation was evaluated by direct cell counting and bromodeoxyuridine (BrdU) labeling. Cell cycle distribution and apoptosis were examined by flow cytometry, and the inhibition rate (IR) by vinorebline (NVB) was determined by MTT assay. The results showed that after transfection of pcDNA3-Plk1 into A549 cells, the e.xpression levels of Plk1 mRNA and protein were greatly decreased. In pcDNA3-Plk1 transfected groups, abnormal morphological changes of cells and growth inhibition were observed, and the BrdU labeling index was significantly lower than in the control groups (P＜0.05). Cells in pcDNA3-Plk1 transfected groups were arresed in G2/M phase and apoptosis was detectable 72 h post transfection. IR induced by vinorebline in pcDNA3-Plk1 transfected groups was significantly higher than in other groups.These data suggested that antisense RNA targeting Pikl could suppress the Plkl expression, and therefore, significantly inhibit cell proliferation and induce cell cycle arrest and apoptosis. Moreover,it sensitized lung cancer cells to chemotherapy.