Effect of HCMV on p38MAPK, apoptosis and cell cycle of human glioma U251 cells.
- Author:
Li-yu CHEN
1
;
Min LUO
;
Tai-cun LI
;
Gan DAI
;
Min-hua LUO
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Blotting, Western; Cell Cycle; Cell Line, Tumor; Cytomegalovirus; isolation & purification; Cytomegalovirus Infections; metabolism; physiopathology; Flow Cytometry; Glioma; metabolism; microbiology; pathology; Humans; MAP Kinase Signaling System; Phosphorylation; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Chinese Journal of Pediatrics 2006;44(10):778-781
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the changes of p38MAPK expressions, the frequency of apoptosis and the distribution of cell cycle of hunan Glioma U251 cells after HCMV infection.
METHODSThe expression of total p38 (both phosphorylated and nonphosphorylated p38) and phosphorylated p38 in U251 cells were detected by Western blotting at 15 min, 30 min, 1 h, 6 h, 10 h, 16 h, 24 h, 36 h and 48 h after HCMV infection. The apoptosis percentage and the cell cycle distribution of U251 cells at 2 d, 5 d and 7 d after HCMV infection were detected by flow cytometry (FCM).
RESULTSThe results of Western blotting demonstrated that a strong increase in phosphorylated p38 was detected from 6 h to 10 h after HCMV infection, with mean gray scales 186.33 +/- 7.51 (t = 5.37, P < 0.01) and 188.00 +/- 7.02 (t = 5.26, P < 0.01 for all) at 6 h and 10 h, respectively, and p38 phosphorylation decreased to the basic level at 16 h after HCMV infection. But the overall levels of p38 protein were not significantly altered during the course of infection. FCM analysis showed that HCMV could significantly increase the apoptotic rates of U251 cells compared with controls (t = 10.84, P < 0.01), and the apoptotic percentages of the cells reached to peak [(10.18 +/- 1.24)%] at 5 d after HCMV infection. The data of FCM showed that HCMV could decrease the number of U251 cells in G1 phase and arrest the cells in S and G2 phase. The numbers of G1 phase U251 cells were significantly lowered to (56.50 +/- 2.57)% (t = 26.45, P < 0.01), (62.33 +/- 2.64)% (t = 21.20, P < 0.01) and (67.45 +/- 4.44)% (t = 10.61, P < 0.01), respectively at 2 d, 5 d and 7 d after infection.
CONCLUSIONHCMV could activate p38MAPK pathway and trigger apoptosis and interfere cell cycle in U251 cells.