دورية أكاديمية
أعرض في EDS

Methamphetamine Dysregulates Macrophage Functions and Autophagy to Mediate HIV Neuropathogenesis.

التفاصيل البيبلوغرافية
العنوان: Methamphetamine Dysregulates Macrophage Functions and Autophagy to Mediate HIV Neuropathogenesis.
المؤلفون: Barbaro JM; Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA., Sidoli S; Department of Biochemistry, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA., Cuervo AM; Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA., Berman JW; Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA.; Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA.
المصدر: Biomedicines [Biomedicines] 2022 May 27; Vol. 10 (6). Date of Electronic Publication: 2022 May 27.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI AG Country of Publication: Switzerland NLM ID: 101691304 Publication Model: Electronic Cited Medium: Print ISSN: 2227-9059 (Print) Linking ISSN: 22279059 NLM ISO Abbreviation: Biomedicines Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI AG, [2013]-
مستخلص: HIV-neurocognitive impairment (HIV-NCI) can be a debilitating condition for people with HIV (PWH), despite the success of antiretroviral therapy (ART). Substance use disorder is often a comorbidity with HIV infection. The use of methamphetamine (meth) increases systemic inflammation and CNS damage in PWH. Meth may also increase neuropathogenesis through the functional dysregulation of cells that harbor HIV. Perivascular macrophages are long-lived reservoirs for HIV in the CNS. The impaired clearance of extracellular debris and increased release of reactive oxygen species (ROS) by HIV-infected macrophages cause neurotoxicity. Macroautophagy is a vital intracellular pathway that can regulate, in part, these deleterious processes. We found in HIV-infected primary human macrophages that meth inhibits phagocytosis of aggregated amyloid-β, increases total ROS, and dysregulates autophagic processes. Treatment with widely prescribed ART drugs had minimal effects, although there may be an improvement in phagocytosis when co-administered with meth. Pharmacologically inhibited lysosomal degradation, but not induction of autophagy, further increased ROS in response to meth. Using mass spectrometry, we identified the differentially expressed proteins in meth-treated, HIV-infected macrophages that participate in phagocytosis, mitochondrial function, redox metabolism, and autophagy. Significantly altered proteins may be novel targets for interventional strategies that restore functional homeostasis in HIV-infected macrophages to improve neurocognition in people with HIV-NCI using meth.
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معلومات مُعتمدة: P30AG038072 United States AG NIA NIH HHS; S10 OD030286 United States OD NIH HHS; RF1 AG054108 United States AG NIA NIH HHS; F30 DA053118 United States DA NIDA NIH HHS; R01DA048609 United States DA NIDA NIH HHS; P01 AG031782 United States AG NIA NIH HHS; T32GM007288-44 United States GM NIGMS NIH HHS; National Institute on Drug Abuse United States DA NIDA NIH HHS; P30CA013330 United States CA NCI NIH HHS; F30DA053118 United States DA NIDA NIH HHS; P30 AG038072 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: HIV-NCI; ROS; autophagy; macrophage; methamphetamine; phagocytosis; proteomics
تواريخ الأحداث: Date Created: 20220624 Latest Revision: 20230701
رمز التحديث: 20230701
مُعرف محوري في PubMed: PMC9220012
DOI: 10.3390/biomedicines10061257
PMID: 35740279
قاعدة البيانات: MEDLINE
الوصف
تدمد:2227-9059
DOI:10.3390/biomedicines10061257