作者: T. Finkel , F. Shawl , S. E. Epstein , E. Speir , E. S. Huang
DOI:
关键词: Restenosis 、 Suppressor 、 Human cytomegalovirus 、 Atherectomy 、 Wild type 、 Coronary restenosis 、 Cancer research 、 Angioplasty 、 Medicine 、 Cell
摘要: 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 restenosis; its causes remain unknown. The results this study implicate human cytomegalovirus (HCMV) and HCMV-induced abnormalities p53 function restenosis process. Almost 40% lesions, obtained by atherectomy, demonstrated increased SMC levels immunopositivity; sequencing revealed be wild type. A strong correlation was found between immunopositivity presence HCMV DNA. Moreover, IE84 protein co-immunoprecipitates with p53, transcriptional capacity is reduced IE84. Thus, may play a causal role restenosis, which at least partly mediated inhibiting suppressor effects.