The Mechanism of Murine Cytomegalovirus Infection Contributing to Atherogenesis in Apolipoprotein E Knockout Mice
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    Abstract:

    Aim To study the immunologic injury mechanism of atherogenesis by murine cytomegalovirus(MCMV) infection. Methods Animal model of atherosclerosis(C57BL/6) with apolipoprotein E knockout mice were randomized to four groups: control group,hypercholesterol diet group,MCMV infection group,MCMV infection add hypercholesterol diet group,respectively.Mice from each group were sacrificed in different period.Portions of aortas were kept in-80℃.The expression of monocyte chemoattractant protein-1(MCP-1),growth-related oncogene-α(GRO-α),fractalkine(FKN) and regulated activation normal T cell expressed and secreted(RANTES) in aortas were detected by RT-PCR and immunohistochemistry. Results In the 8th week,the expression of GRO-α in aorta tissues was significant by CMV infection,and the expression of FKN,RANTES and MCP-1 was induced.The expression of FKN was more significant in MCMV infection add hypercholesterol diet group than other groups.In the 12th week,the expression of FKN and RANTES was marked than others.Immunohistochemistry staining also showed that the expression of MCP-1,GRO-α and FKN was enhanced in atherosclerotic lesion,but expression of FKN was variable,and correlated with the atherosclerotic plaque. Conclusion MCMV infection could contribute to atherogenesis by inducing the expression of chemokines and enhance the migration of inflammatory cells.

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CHEN Rui-Zhen, XIONG Si-Dong, XU Cong-Feng, YANG Ying-Zhen, ZOU Yun-Zeng, GE Jun-Bo, and CHEN Hao-Zhu. The Mechanism of Murine Cytomegalovirus Infection Contributing to Atherogenesis in Apolipoprotein E Knockout Mice[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2008,16(8):589-592.

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History
  • Received:May 05,2008
  • Revised:July 29,2008
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