ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of Cyclin A1 on the proliferation of SKM-1 cells and its underlying role in myelodysplastic syndrome (MDS).</p><p><b>METHODS</b>Cyclin A1 was knocked down with its small interfering RNA (siRNA). The efficiency of siRNA transfection was measured by Western blot and RT-PCR. Then the proliferation of SKM-1 cells and the expression of CDK2,RUNX1 and SRSF2 with and without knockdown of Cyclin A1 recorded and analysed respectively.</p><p><b>RESULTS</b>Cyclin A1 was knocked down by siRNA after transfected for 48 h. The kncokdown of Cyclin A1 inhibited the proliferation of SKM-1 cells and down-regulated the expression of CDK2, RUNX1 and SRSF2, and these effects were at least partially mediated through RUNX1 and SRSF2 signaling pathway.</p><p><b>CONCLUSION</b>Cyclin A1 plays an important role in the proliferation of SKM-1 cells. These findings provide new insights into the pathogenesis of MDS, and it may be a potential target in the treatment of MDS.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression and pathobiological implications of angiotensin II type 1 receptor (AT1R) in development of myocardial fibrosis of rats.</p><p><b>METHODS</b>Rat myocardial necrosis model was established using isoproterenol injection (15 mg/kg). Rat serum aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzymes (CK-MB) were detected by MD-100 automatic biochemical analyzer. Masson staining was used to evaluate the morphological changes. The expression of AT1R protein was determined by immunohistochemistry and its mRNA expression was analyzed by RT-PCR. The expression of collage type I and III was determined by immunohistochemistry.</p><p><b>RESULTS</b>Serum LDH, CK and CK-MB reached their peaks at 4 h (chi2 = 16.90, P < 0.05), and AST achieved its peak in 6 h (chi2 = 16.90, P < 0.05). AT1R mRNA expression was increased 2 - 12 h after isoproterenol injection, but no statistical significance (P > 0.05) was observed comparing with the control. However, a significant AT1R mRNA increase was present at 24 h and decreased gradually after 48 h, and back to the control level after 3 weeks. Protein expression of AT1R increased proportionally with the severity of the fibrosis.</p><p><b>CONCLUSIONS</b>AT1R mRNA and protein expressions increase significantly during myocardial ischemia, and is closely correlated with the fibrosis. These findings indicate that AT1R may play an important role in the pathogenesis of myocardial fibrosis.</p>