ABSTRACT
Objective To investigate the effect of alkaline phosphatase liver / bone / kidney (ALPL) overexpression on ventricular remodeling after acute myocardial infarction (MI). Methods Thirty six 8-week-old male C57BL / 6 J mice were randomly divided into sham group(sham), MI group (MI+Adv-EGFP) and ALPL overexpression group (MI+ Adv-ALPL) with 12 mice in each group. Two weeks after MI, cardiac function of mice was detected by echocardiography, pathological changes was detected by HE staining. ALPL mRNA expression in mouse heart was detected by Real-time PCR. The levels of ALPL, α- smooth muscle actin (α-SMA),collagen I (ColI) and collagen III (ColIII) protein were detected by Western blotting. The collagen volume fraction (CVF) and the ratio of Col I / Col III were measured by polarizing method with Sirius red staining. Results Compared with MI+Adv-EGFP group, the left ventricular ejection fraction (LVEF) (%) and left ventricular fractional shortening (LVFS) (%) of the heart in MI+Adv-ALPL group were reduced significantly (P < 0. 05). Hearts in the ALPL overexpression group showed myocardial fiber broken, and disordered and fibrous scars were obvious in myocardial infarction area. The expression of ALPL and the expression of α-SMA, ColI and ColIII protein in MI+Adv-ALPL group increased significantly (P<0. 05), and the proportion of ColI / ColIII in MI+Adv-ALPL group increased significantly (P<0. 05).Compared with MI+Adv-EGFP group, the CVF and the proportion of the ratio of ColI / ColIII in the MI+Adv-ALPL group increased significantly (P<0. 05). Conclusion ALPL overexpression can promote the ventricular pathological remodeling after acute myocardial infarction in mice.
ABSTRACT
AIM: To investigate the regulatory effects of microRNA(miR)-195 on the biological behaviors, such as viability,apoptosis and migration, of lung cancer A549 cells, and to explore the related mechanisms.METH-ODS:After miR-195 mimics were transfected into the A549 cells,the cell viability, cell cycle distribution and apoptosis were measured by CCK-8 assay and flow cytometry.Transwell assay was used to detect cell migration ability.Furthermore, the protein levels of cyclin D1,CDK2,Bcl-2 and p-Rb/Rb were determined by Western blot.Dual-luciferase reporter as-say was used to screen and identify the possible target genes of miR-195.RESULTS: Over-expression of miR-195 in the A549 cells inhibited the cell viability and induced cell cycle arrest,accompanied with the decrease in the cell migration a-bility and the increase in the apoptotic rate(P<0.05).Furthermore,the protein levels of cyclin D1,CDK2,Bcl-2 and p-Rb were significantly decreased(P<0.05).Dual-luciferase reporter assay demonstrated that MYB was a potential target gene of miR-195.Over-expression of MYB in the A549 cells partially reversed the effects of miR-195 on the cell viability, apoptosis and migration.CONCLUSION: miR-195 inhibits lung cancer A549 cell growth and migration, and promotes cell apoptosis by targeting MYB gene.