Interaction of human cytomegalovirus with p53: possible role in coronary restenosis.
Restenosis occurs in 25-50% of patients. Within 1-6 months after coronary angioplasty, excessive injury-induced smooth muscle cell (SMC) proliferation contributes to the development of restenosis; its causes remain unknown. The results of this study implicate human cytomegalovirus (HCMV) and HCMV-induced abnormalities in p53 function in the restenosis process. Almost 40% of restenosis lesions, obtained by atherectomy, demonstrated increased SMC p53 levels by p53 immunopositivity; sequencing revealed the p53 to be the wild type. A strong correlation was found between p53 immunopositivity and the presence of HCMV DNA. Moreover, the HCMV IE84 protein co-immunoprecipitates with p53, and p53 transcriptional capacity is reduced by IE84. Thus, HCMV may play a causal role in restenosis, which may be at least partly mediated by inhibiting p53 suppressor effects.
Speir
E
E
Cardiology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Huang
E S
ES
Modali
R
R
Leon
M B
MB
Shawl
F
F
Finkel
T
T
Epstein
S E
SE
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology / Q000628:therapy / Q000821:virology*; D003587:Cytomegalovirus / Q000235:genetics* / Q000472:pathogenicity; D003586:Cytomegalovirus Infections / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D015967:Gene Expression Regulation, Viral; D016679:Genome, Viral; D006801:Humans; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012008:Recurrence; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000502:physiology*; D014775:Virus Activation / Q000502:physiology*
D016159:Tumor Suppressor Protein p53