Influence of human cytomegalovirus infection on cell cycle and replication licensing factor Cdt1 in human embryonic lung fibroblastic cells.
- Author:
Ping-Yang CHEN
1
;
Shu-Yuan YAN
;
Mei-Bing QIU
;
Zong-De XIE
;
Shui-Ping LIU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Cycle; Cell Cycle Proteins; genetics; Cells, Cultured; Cytomegalovirus; pathogenicity; Embryo, Mammalian; cytology; Fibroblasts; cytology; metabolism; Humans; Lung; cytology; metabolism; RNA, Messenger; analysis
- From: Chinese Journal of Contemporary Pediatrics 2007;9(6):580-582
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the influence of human cytomegalovirus (HCMV) infection on cell cycle and the expression of replication licensing factor Cdt1 in human embryonic lung fibroblastic (HEL) cells and to explore the pathogenesis of HCMV infection.
METHODSHEL cells were synchronized in the G0/G1 phase by the serum starvation method. The synchronized HEL cells were infected with HCMV, and those that were not subjected to HCMV infection were used as the control group. The HEL cells were harvested at 12, 24, 48, 72 and 96 hrs of HCMV infection. The cell cycle of HEL cells was detected by the flow cytometry. The expression of Cdt1 mRNA in HEL cells was determined by reverse transcription-polymerase chain reaction (RT-PCR).
RESULTSThe cells in the G1 phase in the control group was significantly more than in the HCMV-infected group 12 and 24 hrs after infection (P < 0.01). The expression of Cdt1 mRNA in the HCMV-infected group was significantly lower 12 and 24 hrs after infection but increased significantly 48 hrs after infection compared with the control group (P < 0.05). The expression of Cdt1 mRNA reached a peak at 12 hrs of infection in the control group, but at 48 hrs of infection in the HCMV-infected group, which markedly lagged behind the control group.
CONCLUSIONSHCMV infection arrests the cell cycle of HEL cells at the G1 phase. HCMV infection makes Cdt1 expression delay. HCMV infection can interfere cell cycle of HEL cells possibly through affecting the expression of Cdt1.