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• W2050067173 abstract "Methamphetamine (Meth) abuse exacerbates HIV-1-associated neurocognitive disorders (HAND). The underlying mechanism for this effect is not entirely clear but likely involves cooperation between Meth and HIV-1 virotoxins, such as the transactivator of transcription, Tat. HIV-1 Tat mediates damage in the CNS by inducing inflammatory processes including astrogliosis. Wnt/β-catenin signaling regulates survival processes for both neurons and astrocytes. Here, we evaluated the impact of Meth on the Wnt/β-catenin pathway in astrocytes transfected with Tat. Meth and Tat downregulated Wnt/β-catenin signaling by >50%, as measured by TOPflash reporter activity in both an astrocytoma cell line and primary human fetal astrocytes. Meth and Tat also downregulated LEF-1 transcript by >30%. LEF-1 is a key partner of β-catenin to regulate cognate gene expression. Interestingly, estrogen, which induces β-catenin signaling in a cell-type specific manner, at physiological concentrations of 1.5 and 3 nM normalized individual Meth and Tat effects on β-catenin signaling but not their combined effects. These findings suggest that Meth and Tat likely exert different mechanisms to mediate down regulation of β-catenin signaling. The consequences of which may contribute to the pathophysiologic effects of HIV-1 and Meth co-morbidity in the CNS." @default.
• W2050067173 created "2016-06-24" @default.
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• W2050067173 date "2011-07-09" @default.
• W2050067173 modified "2023-10-06" @default.
• W2050067173 title "Methamphetamine and HIV-1 Tat Down Regulate β-catenin Signaling: Implications for Methampetamine Abuse and HIV-1 Co-morbidity" @default.
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• W2050067173 doi "https://doi.org/10.1007/s11481-011-9295-2" @default.
• W2050067173 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3714216" @default.
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