Efficacy of subgroup mouse bone mesenchymal stem cells on mobilizing autologous cardiac stem cells and repairing ischemic myocardial tissue / 中华心血管病杂志

<p><b>OBJECTIVE</b>To search for the bone mesenchymal stem cell (MSC) subgroup which might be more effective on repairing myocardial damage.</p><p><b>METHODS</b>In this experiment, four MSC subgroups were defined based on the surface differentiation antigen detection of mouse bone mesenchymal stem cells (mBMSCs): SCA-1(+)/CD45(+)/CD31(+), SCA-1(+)/CD45(+)/CD31(-), SCA-1(+)/CD45(-)/CD31(-) and SCA-1(+)/CD45(-)/CD31(+). These subgroup cells and unselected mBMSCs were injected into infarcted mouse via tail vein. Echocardiographic heart function measurement and in vivo DiR-labeled stem cells imaging were performed at 48 h after injection. In situ C-kit (a flag antigen of cardiac stem cells) and cardiac-specific differentiation antigen immunohistochemistry detection was made in the infarcted myocardium.</p><p><b>RESULTS</b>The capacity of the SCA-1(+)/CD45(+)/CD31(+) cells on improving heart function was significantly higher than other cell groups (all P < 0.05). In vivo imaging showed that the mean fluorescence intensity of the SCA-1(+)/CD45(+)/CD31(+) cells was also higher than other cell groups (all P < 0.05). Number of cardiac stem cells in the infracted myocardium was significantly increased after the injection of all subgroup cells and unsorted mBMSCs cells for 48 h compared untreated infracted myocardium. The capacity of mobilizing cardiac stem cells is as follows: SCA-1(+)/CD45(+)/CD31(+) >SCA-1(+)/CD45(-)/CD31(+) >SCA-1(+)/CD45(-)/CD31(-) >SCA-1(+)/CD45(+)/CD31(-).</p><p><b>CONCLUSION</b>The SCA-1(+)/CD45(+)/CD31(+) subgroups of mBMSCs exhibites the highest capacity to improve cardiac function after myocardial infarction and to mobilize autologous cardiac stem cells compared with other mBMSCs subgroups and unsorted mBMSCs cells.</p>

Expression of PNMA5 in hepatocellular carcinoma tissues and its function / 肿瘤

Objective: To study the expression of function-unknown PNMA5 gene in hepatocellular carcinoma (HCC) and its relationship with proliferation of HCC. Methods: PNMA5 was over-expressed in HCC analyzed by gene expression profiling. We investigated the expression of PNMA5 through RT-PCR and real-time fluorescent quantitative PCR (RFQ-PCR) in normal liver tissues, HCC, and adjacent non-cancerous liver tissues (non-HCC). PNMA5 gene was silenced in Focus and PLC liver cancer cells by using RNA interference technology. The changes in cell growth curve were quantitatively analyzed by performing CCK-8 experiment after silencing the endogenous PNMA5 gene expression. Results: PNMA5 was mainly expressed in testis, ovary, and brain tissues out of the 14 kinds of normal human tissues. PNMA5 mRNA was significantly up-regulated in 42% (5/12) HCC specimens, which was 2-fold higher than that in non-HCCs (P < 0.05). Interestingly, the growth of Focus and PLC cells was markedly inhibited after silencing PNMA5 gene expression (P < 0.01), and the number of tumor cells progressing through G1 and entering S phase was significantly decreased as compared with the control cells transfected with siRNA-NC (P < 0.01). Conclusion: PNMA5 plays an important role in maintaining the malignant phenotype of HCC. It may be a novel tumor-testis associated gene. Further investigation of its function may help to find the new mechanism for the HCC tumorigenesis. PNMA5 may become a new candidate target in HCC treatment.