Effect of simvastatin on phosphatase and tensin homologue deleted on chromosome ten and β-catenin of rabbits with chronic heart failure / 新乡医学院学报

Objective To study the effect of simvastatin on the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and β-catenin in myocardial cells of rabbits with chronic heart failure (CHF).Methods Twenty-four male New Zealand rabbits were randomly divided into control group,CHF model group and simvastatin treatment group,with 8 rabbits in each group.The rabbits in CHF model group and simvastatin treatment group were injected with adriamycin (2.0 mg · kg-1) ria ear rein once a week for six weeks,and from the seventh week were injected with adriamycin (1.5 mg · kg-1)once a week for another six weeks to establish the CHF model;the rabbits in control group were injected with the same volume saline.The rabbits in simvastatin treatment group were given simvastatin (1.5 mg · kg-1 · d-1) by intragastric administration at the time point of first injection of adriamycin for 12 weeks;the rabbits in CHF model group and control group were given the same volume saline for 12 weeks.The left ventricular structure and function were determined by color doppler uhrasonography after the modeling.Then the rabbits were sacrificed and the left ventricular walls were taken to observe the changes of myocardial cell structures by hematoxylin-eosin staining.The positive expression rate of PTEN and β-catenin protein was calculated by immunohistochemistry staining.The expression of PTEN and β-catenin mRNA was detected real-time quantitative polymerase chain reaction.Results Compared with the control group,the left ventricular end-systolic dimension (LVESD),left ventricular end-diastolic dimension(LVEDD) were increased and the left ventricular ejection fraction(LVEF) was decreased in the CHF model group and simvastatin treatment group(P ＜ 0.05).Compared with the CHF model group,the LVESD,LVEDD were decreased and the LVEF was increased in the simvastatin treatment group(P ＜ 0.05).The positive expression rate of PTEN protein in myocardial cells of rabbits in control group,CHF model group and simvastatin treatment group was (16.36 ± 0.54) ％,(41.63 + 0.72) ％ and (24.17 ± 0.51) ％ respectively;the positive expression rate of β-catenin protein in myocardial cells of rabbits in control group,CHF model group and simvastatin treatment group was (21.73 ± 0.46)％,(52.26 ±+ 0.72) ％ and (38.42 + 0.56) ％ respectively.The positive expression rates of PTEN and β-catenin protein in myocardial cells of rabbits in CHF model group and simvastatin treatment group were significanlty higher than those in the control group(P ＜ 0.05);the positive expression rates of PTEN and β-catenin protein of myocardial cell in simvastatin treatment group were significantly lower than those in the CHF model group (P ＜ 0.05).The epression of PTEN mRNA and β-catenin mRNA in myocardial cells of rabbits in control group,CHF model group and simvastatin treatment group was 1.91 ± 0.30,4.61 ± 0.71,3.49 ± 0.64 and 1.51 ± 0.21,2.48 ± 0.34,1.51 ±+ 0.25.The expression of PTEN and β-catenin mRNA in myocardial cells of rabbits in CHF model group and simvastatin treatment group were significanlty higher than those in the control group (P ＜ 0.05);the expression of PTEN and β-catenin mRNA in myocardial cells of rabbits in simvastatin treatment group were significantly lower than those in the CHF model group (P ＜ 0.05).Conclusion Simvastatin can inhibit myocardial apoptosis,improve cardiac function of CHF rabbits.It may be related to inhibiting the expression of PTEN and β-catenin.

Effects of PTEN on the migration and invasion of endometrial carcinoma cells / 中国癌症杂志

Background and purpose: Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) gene is a kind of tumor suppressors, which has been reported to be underexpressed in endometrial carcinoma (EC) tissues by several reports. However, the biological effects and possible mechanisms of PTEN on EC have been known less. In this study, we tried to investigate the effects and possible mechanisms of PTEN on the invasion and migration of endometrial carcinoma cells and to provide a potential target for endometrial carcinoma therapy. Methods:The recombinant plasmid pIRES2-ZsGreen1-PTEN was rebuilt by gene recombination technology;The plasmid was transferred into HEC-1B cells and the cells transfected with pIRES2-ZsGreen1 plasmid were used as control;The expression of PTEN was observed by fluorescence microscope and Western blot assay;Cell migration and invasion was determined by the wound healing assay, transwell migration and invasion assays respectively;The Western blot analysis was performed to detect the expression of ATP-dependent tyrosine kinase (AKT), phosphorylated-AKT (p-AKT) and matrix metalloproteinase-2 (MMP-2). Results:The agarose gel electrophoresis showed a stripe of 1.2 kb which was same to PTEN cDNA;The sequence analysis showed the PCR products owned the same sequence with the coding region of PTEN cDNA in GenBank, suggesting the recombinant plasmid was constructed successfully;The green light of cells observed by fluorescence microscope and the Western blot analysis showed the expression of PTEN was upregulated in the cells transfected with the recombinant plasmid, suggesting the plasmid expressed successfully in HEC-1B cells;The wound healing assay as well as transwell migration assay showed ectopic expression of PTEN suppressed cell migration;The invasive capacity of HEC-1B cells was significantly decreased upon transfection with PTEN plasmid compared to control and untreated groups;Moreover, compared with the control groups, the expression of p-AKT and MMP-2 was downregulated, while there was no significant alteration of the expression of AKT. Conclusion:PTEN could suppress cell migratory and invasive ability of endometrial carcinoma cells by suppressing the phosphorylation of AKT followed by the decrease of MMP-2.

Over-expression of PTEN Involved in Troglitazone-induced Apoptosis in Human Osteosarcoma Cells / 대한골관절종양학회지

PURPOSE: We investigated the effects of phosphatase and tensin homologue deleted on chromosome 10 gene phosphatase and tensin homologue deleted on chromosome 10 gene (PTEN) expression on the cell proliferation and on the responsiveness of troglitazone in osteosarcoma cells. MATERIALS AND METHODS: Western blotting alnalysis was performed to detect the expression of PTEN in U-2OS cells treated with troglitazone. WST (water-soluble tetrazolium) assay was used to evaluate cell proliferation. Flow cytometry was used to determine cell apoptosis. Further, transfection of wild-type PTEN plasmid DNA was used to upregulate PTEN expression. RESULTS: Troglitazone treatment induced growth inhibition of U2-OS cells in a dose- and time-dependent manner. Troglitazone increased the expression of PTEN in a dose-dependent manner. PTEN upregulation induced by troglitazone treatment resulted in cell growth inhibition and apoptosis in U-2OS cells. PTEN over-expression by plasmid transfection enhanced these effects of troglitazone. Moreover, no changes were observed in the mutant type-PTEN group. CONCLUSION: Upregulation of PTEN is involved in the inhibition of cell growth and induction of cell apoptosis by troglitazone. Further, PTEN over-expression can cause cell growth inhibition in osteosarcoma cells and these cell growth inhibitions could be enhance by troglitazone treatment.

Function of Phosphatase and Tensin Homologue Deleted on Chromosome 10 in Formation and Maintenance of Neuronal Circuits in Brain / 实用儿科临床杂志

Phosphatase and tensin homologue deleted on chromosome 10(PTEN) is a tumor suppressor which can inhibit proliferation and migration and control apoptosis in a number of cell types,mainly through inhibiting the phosphoinositide 3-kinase(PI3K) signaling pathway.A number of in vitro and in vivo studies has been instrumental in uncovering a direct correlation between deregulated PTEN/PI3K signaling and changes in neuronal morphogenesis,which is likely to have profound bearings upon the pathogenesis of neurological symptoms.This review outlines recent work on the function of PTEN during the formation and maintenance of neuronal circuits in the brain.

Regulation of Phosphatase and Tensin Homology Deleted on Chromosome 10 / 实用儿科临床杂志

Phosphatase and tensin homology deleted on chromosome 10 (PTEN) is a tumor suppressor with dual protein and lipid phosphatase activity.PTEN is involved multisystem diseases and cancer,though the mechanisms of PTEN regulation are far from clear.Recent advances concerning regulation of PTEN including protein-protein interaction,phosphorylation,ubiquitination,oxidation and acetylation will be discussed.

Correlation between Akt phosphorylation and loss of PTEN protein expression in non-small-cell lung cancer / 中国癌症杂志

Purpose:To clarify roles of overexpression of phosphorylated Akt(p-Akt) and loss of phosphatase and tensin homologue deleted on chromosome 10(PTEN) expression in biological behavior of non-small-cell lung cancer(NSCLC). Methods:Immunohistochemical staining was used to determine the expression of p-Akt and PTEN in 20 cases of normal lung tissues and 102 patients with NSCLC.Results:Negative p-Akt expression and positive PTEN expression were found in normal lung tissues, while the positive incidences of p-Akt expresssion and loss of incidences of PTEN expresssion in NSCLC were 41.2% (42/102) and 46.1% (47/102)respectivtly.The overexpression of p-Akt and loss of PTEN expression were correlated to degree of differention of cancer, metastasis(including lymph node), and clinical stages. A significant negative correlation was observed between expression of p-Akt and PTEN(Phi r=-0.425,P