【摘 要】
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Despite the success of combined antiretroviral therapy in recent years,the prevalence of human immunodeficiency virus (HIV)-associated neurocognitive disorders in people living with HIV-1 is increasing,significantly reducing the health-related quality of
【机 构】
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Laboratory of Medical Molecular Virology, School of Medicine, Nankai University, Tianjin 300071, Chi
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Despite the success of combined antiretroviral therapy in recent years,the prevalence of human immunodeficiency virus (HIV)-associated neurocognitive disorders in people living with HIV-1 is increasing,significantly reducing the health-related quality of their lives.Although neurons cannot be infected by HIV-1,shed viral proteins such as transactivator of transcription (Tat) can cause dendritic damage.However,the detailed molecular mechanism of Tat-induced neuronal impairment remains unknown.In this study,we first showed that recombinant Tat (1-72 aa) induced neurotoxicity in primary cultured mouse neurons.Second,exposure to Tat1-72 was shown to reduce the length and number of dendrites in cultured neurons.Third,Tat1-72 (0-6 h) modulates protein phosphatase 1 (PP1) expression and enhances its activity by decreasing the phosphorylation level of PP1 at Thr320.Finally,Tat1-72 (24 h) downregulates CREB activity and CREB-mediated gene (BDNF,c-fos,Egr-1) expression.Together,these findings suggest that Tat1-72 might impair cognitive function by regulating the activity of PP1 and the CREB/BDNF pathway.
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