Effect Of HCMV On P38MAPK And Apoptosis Of Human Gliomatous Cells U251 Strain

Objective: To elucidate the pathogenesis of human cytomegalovirus (HCMV), we studied the activation of p38MAPK pathway after HCMV infection and the relationship between HCMV infection and the frequency of apoptosis of hunan Gliomatous cells U 251 strain.Methods:HCMV-LA in U251 cells infected with HCMV were detected by immuneohistochemistry staining; The expression of total p38 (both phosphorylated and nonphosphorylated p38) and phosphorylated p38 at different times in U251 cells after HCMV infection was detected by western blotting; Because several reports have demonstred that p38 MAPK family promoted apoptosis,we have detected the apoptosis and the cell cycle distribution of U251 cells after HCMV infection by flow cytometry.Results: (l)Five days after HCMV infection , HCMV-LA was detected in the cytoplasm of U251 cells; (2) Using western blotting, our results demonstrated that a strong increase in p38 phosphorylation was detected by 6 hpi, and p38 phosphorylation decreased between 10 and 16 hpi. Western blot analysis using an antibody which recognizes both phosphorylated and nonphosphorylated p38 demonstrated that the overalllevels of p38 protein were not significantly altered during the course of infection, suggesting that the increase in phosphorylated p38 was not due to an elevation in the amount of p38 analyzed; (3) The data of FCM showed that HCMV could significantly increased the apoptosis rates of U251 cells infected with HCMV compared with control and that HCMV could decrease the number of U251 cells in Gl phase and arrest U251 cells in S and G2 phase.Conclusion: HCMV could active p38MAPK pathway and trigger apoptosis and interfere cell cycle in U251 cells.