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Tytuł pozycji:

HIV-1 Tat-mediated astrocytic amyloidosis involves the HIF-1α/lncRNA BACE1-AS axis.

Tytuł :
HIV-1 Tat-mediated astrocytic amyloidosis involves the HIF-1α/lncRNA BACE1-AS axis.
Autorzy :
Sil S; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Hu G; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Liao K; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Niu F; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Callen S; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Periyasamy P; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Fox HS; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Buch S; Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
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Źródło :
PLoS biology [PLoS Biol] 2020 May 26; Vol. 18 (5), pp. e3000660. Date of Electronic Publication: 2020 May 26 (Print Publication: 2020).
Typ publikacji :
Journal Article; Research Support, N.I.H., Extramural
Język :
English
Imprint Name(s) :
Original Publication: San Francisco, CA : Public Library of Science, [2003]-
MeSH Terms :
Amyloidosis/*virology
Astrocytes/*metabolism
HIV Infections/*complications
Neurocognitive Disorders/*virology
tat Gene Products, Human Immunodeficiency Virus/*metabolism
Amyloid beta-Peptides/metabolism ; Amyloidosis/metabolism ; Animals ; Brain/metabolism ; Cells, Cultured ; HIV Infections/metabolism ; HIV-1 ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Macaca mulatta ; Middle Aged ; Neurocognitive Disorders/metabolism ; Peptide Fragments/metabolism ; RNA, Long Noncoding/metabolism ; Up-Regulation
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Grant Information :
R01 MH106425 United States MH NIMH NIH HHS; R25 MH080661 United States MH NIMH NIH HHS
Substance Nomenclature :
0 (Amyloid beta-Peptides)
0 (BACE1-AS long non-coding RNA, human)
0 (HIF1A protein, human)
0 (Hypoxia-Inducible Factor 1, alpha Subunit)
0 (Peptide Fragments)
0 (RNA, Long Noncoding)
0 (amyloid beta-protein (1-42))
0 (tat Gene Products, Human Immunodeficiency Virus)
Entry Date(s) :
Date Created: 20200527 Date Completed: 20200720 Latest Revision: 20200720
Update Code :
20201023
PubMed Central ID :
PMC7274476
DOI :
10.1371/journal.pbio.3000660
PMID :
32453744
Czasopismo naukowe
Increased life expectancy of patients diagnosed with HIV in the current era of antiretroviral therapy is unfortunately accompanied with the prevalence of HIV-associated neurocognitive disorders (HANDs) and risk of comorbidities such as Alzheimer-like pathology. HIV-1 transactivator of transcription (Tat) protein has been shown to induce the production of toxic neuronal amyloid protein and also enhance neurotoxicity. The contribution of astrocytes in Tat-mediated amyloidosis remains an enigma. We report here, in simian immunodeficiency virus (SIV)+ rhesus macaques and patients diagnosed with HIV, brain region-specific up-regulation of amyloid precursor protein (APP) and Aβ (40 and 42) in astrocytes. In addition, we find increased expression of β-site cleaving enzyme (BACE1), APP, and Aβ in human primary astrocytes (HPAs) exposed to Tat. Mechanisms involved up-regulation of hypoxia-inducible factor (HIF-1α), its translocation and binding to the long noncoding RNA (lncRNA) BACE1-antisense transcript (BACE1-AS), resulting, in turn, in the formation of the BACE1-AS/BACE1 RNA complex, subsequently leading to increased BACE1 protein, and activity and generation of Aβ-42. Gene silencing approaches confirmed the regulatory role of HIF-1α in BACE1-AS/BACE1 in Tat-mediated amyloidosis. This is the first report implicating the role of the HIF-1α/lncRNABACE1-AS/BACE1 axis in Tat-mediated induction of astrocytic amyloidosis, which could be targeted as adjunctive therapies for HAND-associated Alzheimer-like comorbidity.
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