Abstract：
:Microglia are activated in humans following infection with human immunodeficiency virus (HIV), and brain inflammation is thought to be involved in neuronal injury and dysfunction during HIV infection. Numerous studies indicate a role for the HIV regulatory protein Tat in HIV-related inflammatory and neurodegenerative processes, although the specific effects of Tat on microglial activation, and the signal transduction mechanisms thereof, have not been elucidated. In the present study, we document the effects of Tat on microglial activation and characterize the signal transduction pathways responsible for Tat's pro-inflammatory effects. Application of Tat to N9 microglial cells increased multiple parameters of microglial activation, including superoxide production, phagocytosis, nitric oxide release and TNF alpha release. Tat also caused activation of both p42/p44 mitogen activated protein kinase (MAPK) and NF kappa B pathways. Inhibitor studies revealed that Tat-induced NF kappa B activation was responsible for increased nitrite release, while MAPK activation mediated superoxide release, TNF alpha release, and phagocytosis. Lastly, pre-treatment of microglial cells with physiological concentrations of 17 beta-estradiol suppressed Tat-mediated microglial activation by interfering with Tat-induced MAPK activation. Together, these data elucidate specific components of the microglial response to Tat and suggest that Tat could contribute to the neuropathology associated with HIV infection through microglial promulgation of oxidative stress.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Bruce-Keller AJ,Barger SW,Moss NI,Pham JT,Keller JN,Nath Adoi
10.1046/j.1471-4159.2001.00511.xkeywords:
subject
Has Abstractpub_date
2001-09-01 00:00:00pages
1315-24issue
6eissn
0022-3042issn
1471-4159journal_volume
78pub_type
杂志文章abstract：:Lewy body disease (LBD) development is enhanced by mutations in the GBA gene coding for glucocerebrosidase (GCase). The mechanism of this association is thought to involve an abnormal lysosomal system and we therefore sought to evaluate if lysosomal changes contribute to the pathogenesis of idiopathic LBD. Analysis of...
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更新日期：1990-01-01 00:00:00
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journal_title：Journal of neurochemistry
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doi：10.1111/j.1471-4159.1987.tb05656.x
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1988.tb01044.x
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1990.tb04557.x
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1992.tb08321.x
更新日期：1992-09-01 00:00:00
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doi：10.1111/j.1471-4159.1993.tb13625.x
更新日期：1993-10-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1046/j.1471-4159.1996.66010394.x
更新日期：1996-01-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1046/j.1471-4159.1994.63062295.x
更新日期：1994-12-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章,评审
doi：10.1111/jnc.13532
更新日期：2016-04-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1046/j.1471-4159.1994.62031039.x
更新日期：1994-03-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1989.tb09217.x
更新日期：1989-05-01 00:00:00
abstract：:Poly A(+) messenger RNA (mRNA) was isolated from the brains of 3-week-old mice and translated in a cell-free system derived from wheat germ. Maximal stimulation of the system by brain mRNA was observed at a relatively low K+ concentration (45 mM) and low mRNA concentration (1-10 microgram/ml). The translational system...
journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1980.tb07084.x
更新日期：1980-10-01 00:00:00
abstract：:The accumulation of choline, homocholine, and 4-hydroxybutyltrimethylammonium by rat brain synaptosomes was measured; the choline uptake mechanism transported homocholine but not hydroxybutyltrimethylammonium, which, in addition, did not block choline accumulation. In cats' superior cervical ganglia, preganglionic ner...
journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1981.tb01732.x
更新日期：1981-03-01 00:00:00
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pub_type： 杂志文章
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更新日期：2014-04-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1986.tb13048.x
更新日期：1986-03-01 00:00:00
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更新日期：1991-01-01 00:00:00
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更新日期：1982-05-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1981.tb06310.x
更新日期：1981-12-01 00:00:00
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更新日期：1998-08-01 00:00:00
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pub_type： 杂志文章
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更新日期：1990-08-01 00:00:00
abstract：:Mutations in Parkin, an E3 ligase, which participates in the ubiquitin-proteasome system (UPS), cause juvenile onset Parkinson's disease (PD). Some mutants aggregate upon over-expression, but the effects of such aggregation on the UPS and neuronal survival have not been characterized. We show in this study that transi...
journal_title：Journal of neurochemistry
pub_type： 杂志文章
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更新日期：2007-08-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1988.tb01161.x
更新日期：1988-12-01 00:00:00
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更新日期：2010-06-01 00:00:00
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journal_title：Journal of neurochemistry
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更新日期：1985-11-01 00:00:00
