کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478569 | 1551140 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
GSK3β-activation is a point of convergence for HIV-1 and opiate-mediated interactive neurotoxicity
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کلمات کلیدی
NF-κBdouble-stranded RNA-activated protein kinaseTrans-activator of transcriptionHSF-1FGFsNeuroAIDSVPAPKRGSK3βCARTMAP-2cdk5gp120PSD-95CREBPI3KGAPDHHDACAP-1TAT - تاتNeurodegeneration - تولید نوروژنیکcombination antiretroviral therapy - درمان ضد رتروویروسی ترکیبیHand - دستCNS - دستگاه عصبی مرکزیValproate - سدیم والپرووات central nervous system - سیستم عصبی مرکزیcyclin-dependent kinase 5 - سیکلین وابسته به کیناز 5Fibroblast Growth Factors - عوامل رشد فیبروبلاستHeat shock factor-1 - فاکتور شوک حرارت 1Nuclear factor-kappa B - فاکتور هسته ای-کاپا Bphosphatidylinositol-3-kinase - فسفاتیدیلینواستیل-3-کینازMORs - مورسmorphine - مورفینhistone deacetylase - هیستون داستیلازHIV-1 - ویروس اچ آی وی نوع یکhuman immunodeficiency virus-1 - ویروس نقص ایمنی بدن انسان 1cyclic AMP response element binding protein - پروتئین اتصال دهنده عنصر پاسخ Cyclic AMPactivator protein 1 - پروتئین فعال کننده 1microtubule-associated protein 2 - پروتئین مرتبط با میکروتوبول 2postsynaptic density protein 95 - پروتئین چگالی Postynaptic 95glyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازGlycogen synthase kinase-3β - گلیکوزین سنتاز کیناز 3βGlycoprotein 120 - گلیکوپروتئین 120μ-opioid receptors - گیرنده های μ-opioid
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: GSK3β-activation is a point of convergence for HIV-1 and opiate-mediated interactive neurotoxicity GSK3β-activation is a point of convergence for HIV-1 and opiate-mediated interactive neurotoxicity](/preview/png/8478569.png)
چکیده انگلیسی
Infection of the CNS with HIV-1 occurs rapidly after primary peripheral infection. HIV-1 can induce a wide range of neurological deficits, collectively known as HIV-1-associated neurocognitive disorders. Our previous work has shown that the selected neurotoxic effects induced by individual viral proteins, Tat and gp120, and by HIV+ supernatant are enhanced by co-exposure to morphine. This mimics co-morbid neurological effects observed in opiate-abusing HIV+ patients. Although there is a correlation between opiate drug abuse and progression of HIV-1-associated neurocognitive disorders, the mechanisms underlying interactions between HIV-1 and opiates remain obscure. Previous studies have shown that HIV-1 induces neurotoxic effects through abnormal activation of GSK3β. Interestingly, expression of GSK3β has shown to be elevated in brains of young opiate abusers indicating that GSK3β is also linked to neuropathology seen with opiate-abusing patients. Thus, we hypothesize that GSK3β activation is a point of convergence for HIV- and opiate-mediated interactive neurotoxic effects. Neuronal cultures were treated with supernatant from HIV-1SF162-infected THP-1 cells, in the presence or absence of morphine and GSK3β inhibitors. Our results show that GSK3β inhibitors, including valproate and small molecule inhibitors, significantly reduce HIV-1-mediated neurotoxic outcomes, and also negate interactions with morphine that result in cell death, suggesting that GSK3β-activation is an important point of convergence and a potential therapeutic target for HIV- and opiate-mediated neurocognitive deficits.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 65, March 2015, Pages 11-20
Journal: Molecular and Cellular Neuroscience - Volume 65, March 2015, Pages 11-20
نویسندگان
Ruturaj R. Masvekar, Nazira El-Hage, Kurt F. Hauser, Pamela E. Knapp,