ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Transcription factor FOXO3a mediates apoptosis in HIV-1-infected macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Increased Oxidative Stress and Decreased Sirtuin-3 and FOXO3 Expression Following Carotid Artery Intimal Injury in Hyperlipidemic Yucatan Microswine.Cardiology and cardiovascular medicine · 2024Article
- Article
- FOXO3 Expression in Macrophages Is Lowered by a High-Fat Diet and Regulates Colonic Inflammation and Tumorigenesis.Metabolites · 2022Article
- CounterAKTing HIV: Toward a "Block and Clear" Strategy?Frontiers in cellular and infection microbiology · 2022Review
- Forkhead transcription factor FOXO3a mediates interferon-γ-induced MHC II transcription in macrophages.Immunology · 2019Article
- Small molecule ONC201 inhibits HIV-1 replication in macrophages via FOXO3a and TRAIL.Antiviral research · 2019Article
- Role of FOXO3 Activated by HIV-1 Tat in HIV-Associated Neurocognitive Disorder Neuronal Apoptosis.Frontiers in neuroscience · 2019Article
- HTLV-1 Tax-mediated inhibition of FOXO3a activity is critical for the persistence of terminally differentiated CD4+ T cells.PLoS pathogens · 2014Article
- HIV-induced kidney cell injury: role of ROS-induced downregulated vitamin D receptor.American journal of physiology. Renal physiology · 2012Article
- TRAIL is involved in CpG ODN-mediated anti-apoptotic signals.Oncology reports · 2012Article
- HIV gene expression deactivates redox-sensitive stress response program in mouse tubular cells both in vitro and in vivo.American journal of physiology. Renal physiology · 2012Article
- HIV-1 clade B and C isolates exhibit differential replication: relevance to macrophage-mediated neurotoxicity.Neurotoxicity research · 2011Article
- FOXO3 deficiency leads to increased susceptibility to cigarette smoke-induced inflammation, airspace enlargement, and chronic obstructive pulmonary disease.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- HIV/SIV infection primes monocytes and dendritic cells for apoptosis.PLoS pathogens · 2011Article
- Article
- Toll-like receptor 9-mediated inhibition of apoptosis occurs through suppression of FoxO3a activity and induction of FLIP expression.Experimental & molecular medicine · 2010Article
- Association of Tat with promoters of PTEN and PP2A subunits is key to transcriptional activation of apoptotic pathways in HIV-infected CD4+ T cells.PLoS pathogens · 2010Article
- Forkhead transcription factors in chronic inflammation.The international journal of biochemistry & cell biology · 2010Review
- Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice.The Journal of clinical investigation · 2009Article
- Tumor suppressor FOXO3 participates in the regulation of intestinal inflammation.Laboratory investigation; a journal of technical methods and pathology · 2009Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Macrophages serve as a major reservoir for HIV-1 because a large number of macrophages in the brain and lung are infected with HIV-1 during late stage disease. Recent evidence suggests that those HIV-1-infected macrophages play a key role in contributing to tissue damage in AIDS pathogenesis. Macrophages undergo apoptosis upon HIV-1 infection; however, the mechanisms of this process are not well-defined. Previously, we demonstrated that HIV-1 infection inhibits Akt-1, a critical protein for cell survival of macrophages. In the present study, we investigated the involvement of transcription factor FOXO3a in the regulation of HIV-1-mediated apoptosis in macrophages. HIV-1 infection significantly decreased phosphorylation of FOXO3a and promoted FOXO3a translocation to the nucleus in human monocyte-derived macrophages (MDM). Overexpression of a constitutively active FOXO3a increased DNA fragmentation with decreased cell viability in MDM, whereas a dominant-negative mutant of FOXO3a or small interfering RNA for FOXO3a to knockdown the function of FOXO3a in HIV-1-infected MDM decreased DNA fragmentation and protected macrophages from death in HIV-1-infected MDM. Overexpression of constitutively active Akt-1 increased FOXO3a phosphorylation, suggesting that FOXO3a phosphorylation in human MDM is dependent on Akt-1. We therefore conclude that FOXO3a plays an important role in HIV-1-induced cell death of human macrophage. Understanding the PI3K/Akt-1/FOXO3a pathway and its associated death mechanism in macrophages during HIV-1 infection would lead to identification of potential therapeutic avenues for the treatment of HIV-1 infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.