Objective To observe the dynamic changes of endothelial progenitor cells (EPC)and vascular endothelial growth factor (VEGF) in the patients with acute myocardial infarction (AMI)after percutaneous transluminal coronary intervention (PCI). Methods The level of VEGF before and after PCI in 50 cases with AMI were determined by fluorescence immunoassay and enzyme-linked immunosorbnent assay (ELISA),and the ratio of EPC in flood was checked by flow cytometry.Results The level of EPC was higher after PCI than before PCI [(4.15 ± 0.22)％ vs.(0.59 ±0.02) ％,P＜0.01],and there were positive correlations between EPC and number of coronary artery disease (r=0.45,P ＜ 0.05 ),coronary artery lesions ( r =0.76,P ＜ 0.01 ),left ventricular enddiastolic diameter (r=0.68,P＜0.01),ejection fraction (r=0.75,P＜0.01).The VEGF levels after PCI was increased [(506± 120)μg/L vs.(204±98)μg/L,P＜0.01],and its level was positively related with coronary lesions (r=0.66,P＜0.01),left ventricular ejection fraction(r=0.90,P＜0.01).There was association between rising rates of EPC and VEGF in a short time after PCI within 24 h period (r=0.56,P＜0.01). Conclusions The clinical efficacy and prognosis can be assessed by the changes of VEGF level and EPC ratio before and after PCI operation in AM1 patients.

Objective To observe the effect of brain-derived microvesicles (BDMVs) on cytoskeleton in human umbilical vein endothelial cells (HUVECs).Methods BDMVs were prepared in vitro and identified by transmission electron microscopy and particle size identification.HUVECs were co-cultured with PKH26-1abeled BDMVs for 0.5,1,and 2 h;flow cytometry was used to detect the phagocytosis of HUVECs for BDMVs at different time points.HUVECs cultured in vitro were divided into control group,BDMVs treatment group and nimodipine treatment group;cells in the BDMVs treatment group were given 1.5× 107/mL BDMVs;cells in the nimodipine treatment group were pretreated with 2 μg nimodipine (0.2 mg/mL) for 10 min,and then,given 1.5×107/mL BDMVs.After being stained with rhodamine-labeled phalloidin,the fluorescence intensity and number of stress fibers of fibroactin in HUVECs were observed by laser confocal microscopy.Results BDMVs had complete membrane structure with a diameter of 100-1000 nm under transmission electron microscopy.The proportion of cells phagocytizing BDMVs increased significantly with prolonged incubation time,enjoying significant differences (0.5h:22.7％±1.2％;1 h:52.3％±1.3％;2h:71.6％±1.9％,P＜0.05).Laser confocal microscopy showed that,as compared with the control group,the fluorescence intensity ofcytoskeletal protein was obviously increased and the number of stress fibers increased was obviously larger in the BDMVs treatment group.As compared with those in the BDMVs treatment group,the fluorescence intensity of cytoskeletal protein was decreased and the number of stress fibers was obviously smaller in the nimodipine group.Conclusion The role of BDMVs in phagocytosis of HUVECs becomes stronger as time being prolonged,and BDMVs phagocytosis leads to cytoskeletal remodeling,which can be partially blocked by nimodipine.

Objective: To investigate the differential expression of serum-and-glucocorticoid-inducible-kinase-2 (SGK2) in hepatocellular carcinoma (HCC) and normal liver tissues and the related mechanism mediating signal transduction of GSK-3 β / β catenin in HCC cells. Methods: Twenty pairs of matched HCC and normal tissues were collected and the situation of expression of SGK2 mRNA was detected by real-time fluorescence quantitative PCR. Western blot was used to detect the levels of SGK2 protein in human HCC cell lines (Huh-7, SMMC-7721) and normal human liver cell line (L02). SGK2 siRNA was used to transfect human HCC cell lines (SMMC-7721 and Huh-7), and then the protein expression levels of GSK-3 β/ β - catenin was successfully detected with the above-mentioned transfected cell line by western blot. Measurement data were expressed as mean ± standard deviation (±s), and the Student t -test was used as the statistical method. Results: SGK2 mRNA expression was up-regulated in all 20 HCC samples than that of the expression of matched normal liver tissues. SGK2 protein levels were significantly higher in Huh-7 and SMMC-7721 than normal human liver cell lines (P < 0.01). The downregulation of SGK2 expression in human HCC cell lines (SMMC-7721 and Huh-7) had inhibited the expression of unphosphorylated GSK-3 β. In addition, the downregulation of SGK2 expression in HCC cell lines had decreased the dephosphorylation of β - catenin to prevent degradation of the β - catenin proteasome. Conclusion SGK2 is overexpressed in HCC and mediates GSK-3β/β- catenin signaling in HCC cells.