Proliferation inhibition of astrocytes, neurons, and non-glial cells by intracellularly expressed human immunodeficiency virus type 1 (HIV-1) Tat protein
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Acknowledgements
This work was supported by grants R01NS39804 and R01MH65158 (to J.J.H.) from the National Institutes of Health.
References (20)
- et al.
Effects of HIV-1 Tat protein on ion secretion and on cell proliferation in human intestinal epithelial cells
Gastroenterology
(2003) - et al.
Intracellular human immunodeficiency virus Tat expression in astrocytes promotes astrocyte survival but induces potent neurotoxicity at distant sites via axonal transport
J. Biol. Chem.
(2003) - et al.
Neuropathologies in transgenic mice expressing human immunodeficiency virus type 1 Tat protein under the regulation of the astrocyte-specific glial fibrillary acidic protein promoter and doxycycline
Am. J. Pathol.
(2003) - et al.
HIV-1 Tat elongates the G1 phase and indirectly promotes HIV-1 gene expression in cells of glial origin
J. Biol. Chem.
(1998) - et al.
Is green fluorescent protein toxic to the living cells?
Biochem. Biophys. Res. Commun.
(1999) - et al.
HIV-1 Tat protein-mediated transactivation of the HIV-1 long terminal repeat promoter is potentiated by a novel nuclear Tat-interacting protein of 110 kDa, Tip110
J. Biol. Chem.
(2002) - et al.
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Cell
(1997) - et al.
Release, uptake, and effects of extracellular human immunodeficiency virus type 1 Tat protein on cell growth and viral transactivation
J. Virol.
(1993) - et al.
Tat-expressing Jurkat cells show an increased resistance to different apoptotic stimuli, including acute human immunodeficiency virus-type 1 (HIV-1) infection
Br. J. Haematol.
(1995) - et al.
Transcriptional activation by tetracyclines in mammalian cells
Science
(1995)
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HIV-1 tat promotes lysosomal exocytosis in astrocytes and contributes to astrocyte-mediated tat neurotoxicity
2016, Journal of Biological ChemistryCitation Excerpt :Tat has indeed been detected in and secreted by astrocytes that are latently infected with HIV (9, 25). Tat alters astrocyte growth (21, 22, 26) and induces expression of cytokines and chemokines in astrocytes such as MCP-1, IL-1β, IL-6, RANTES, and CXCL10 (17, 27, 28), which could in turn recruit more macrophages/monocytes and lymphocytes into the CNS (13–16). Studies, including ours, have shown that astrocytes potentiate Tat neurotoxicity (16, 20, 22), probably through Tat-mediated transcriptional activation of glial fibrillary acidic protein (GFAP) expression (29–31).
HIV-1 tat induces unfolded protein response and endoplasmic reticulum stress in astrocytes and causes neurotoxicity through glial fibrillary acidic protein (GFAP) activation and aggregation
2016, Journal of Biological ChemistryCitation Excerpt :Importantly, the activation of astrocytes, also known as astrocytosis, which is characterized by increased accumulation of the intermediate filament GFAP,2 has been a consistent hallmark of HIV/neuroAIDS. GFAP, an astrocyte-specific cell marker, is a critical regulator of Tat neurotoxicity (40–45), defining what is known as astrocyte-mediated Tat neurotoxicity. However, the underlying molecular mechanisms are largely unknown.
Protection against human immunodeficiency virus type 1 Tat neurotoxicity by Ginkgo biloba extract EGb 761 involving glial fibrillary acidic protein
2007, American Journal of PathologyCitation Excerpt :The consensus oligonucleotide sequences were 5′-CGCTTGATGAGTCAGCCGGAA-3′ for AP1, 5′-GATCGAACTGA-CCGCCCGCGGCCCGT-3′ for AP2, 5′-AGTTGAGGGG-ACTTTCCCAGGC-3′ for NF-κB, and 5′-AGAGATTGCC-TGACGTCAGAGAGCTAG-3′ for CREB. Primary murine astrocytes were isolated from 16.5- to 18-day fetuses as described18,19 and maintained in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum, 50 U/ml penicillin, and 50 μg/ml streptomycin in a 37°C, 5% CO2 incubator. The cells were cultured for 9 to 12 days in vitro and then plated in a 24-well plate at a density of 5 × 104 cells/well and treated with EGb 761 at indicated concentrations for 3 days.
The multiple roles of p53 in the pathogenesis of HIV associated dementia
2005, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Additional evidence for a possible role of p53 in the pathogenesis of HAD comes from studies of several CNS cell types engineered to express Tat. In both astrocyte and neuronal cell lines, intra-cellular expression of Tat led to cell cycle arrest and Tat interacted with several known regulators of the cell cycle including p53 [108]. While it is unlikely that either astrocytes or neurons actually express HIV-Tat, several studies have demonstrated that extracellular Tat is rapidly internalized by neurons and astrocytes [109,110].
Astrocyte activation and dysfunction and neuron death by HIV-1 Tat expression in astrocytes
2004, Molecular and Cellular Neuroscience