ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Antiplatelet activity of valproic acid contributes to decreased soluble CD40 ligand production in HIV type 1-infected individuals.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Characterization of platelet-monocyte complexes in HIV-1-infected individuals: possible role in HIV-associated neuroinflammation.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Valproate-Induced Metabolic Syndrome.Biomedicines · 2023Review
- Blood Platelets in Infection: The Multiple Roles of the Platelet Signalling Machinery.International journal of molecular sciences · 2023Review
- The Role of Platelets in the Pathogenesis and Pathophysiology of Adenomyosis.Journal of clinical medicine · 2023Review
- Monocytes complexed to platelets differentiate into functionally deficient dendritic cells.Journal of leukocyte biology · 2021Article
- Thrombocytopenia in Virus Infections.Journal of clinical medicine · 2021Review
- Dynamics of Transforming Growth Factor (TGF)-β Superfamily Cytokine Induction During HIV-1 Infection Are Distinct From Other Innate Cytokines.Frontiers in immunology · 2020Article
- Regulation of platelet-activating factor-induced interleukin-8 expression by protein tyrosine phosphatase 1B.Cell communication and signaling : CCS · 2019Article
- The HIV protease inhibitor, ritonavir, dysregulates human platelet function in vitro.Thrombosis research · 2018Article
- Different resuscitation strategies and novel pharmacologic treatment with valproic acid in traumatic brain injury.Journal of neuroscience research · 2018Review
- Platelets in Immune Response to Virus and Immunopathology of Viral Infections.Frontiers in medicine · 2018Review
- Anti-platelet therapy holds promises in treating adenomyosis: experimental evidence.Reproductive biology and endocrinology : RB&E · 2016Article
- Novel Antiplatelet Activity of Minocycline Involves Inhibition of MLK3-p38 Mitogen Activated Protein Kinase Axis.PloS one · 2016Article
- Soluble CD40-ligand (sCD40L, sCD154) plays an immunosuppressive role via regulatory T cell expansion in HIV infection.Clinical and experimental immunology · 2014Article
- Targeting platelet-derived soluble CD40 ligand: a new treatment strategy for HIV-associated neuroinflammation?Journal of neuroinflammation · 2013Review
- Alterations of platelet function and clot formation kinetics after in vitro exposure to anti-A and -B.Transfusion · 2013Article
- Loss of the cytoskeletal protein Pdlim7 predisposes mice to heart defects and hemostatic dysfunction.PloS one · 2013Article
- Article
- Detection of circulating platelet-monocyte complexes in persons infected with human immunodeficiency virus type-1.Journal of virological methods · 2012Article
- Excess soluble CD40L contributes to blood brain barrier permeability in vivo: implications for HIV-associated neurocognitive disorders.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
CD40L is a type II membrane glycoprotein of the TNF family that is found on activated T cells, B cells, and platelets. We previously reported that the soluble form of this inflammatory mediator (sCD40L) is elevated in the plasma and cerebrospinal fluid of HIV-1-infected, cognitively impaired individuals. In this study, we demonstrate that the mood-stabilizing drug valproic acid (VPA) reduces sCD40L levels in plasma samples of HIV-1-infected patients (n = 23) and in washed human platelets, which are the main source of circulating sCD40L. VPA also inhibited HIV-1 transactivator of transcription-induced release of sCD40L and platelet factor 4 in C57BL/6 mice. The mechanism by which VPA was able to do so was investigated, and we demonstrate that VPA, a known glycogen synthase kinase 3β inhibitor, blocks platelet activating factor-induced activation of glycogen synthase kinase 3β in platelets in a manner that alters sCD40L release from platelets. These data reveal that VPA has antiplatelet activity, and they convey important implications for the potential of VPA as an adjunct therapy not only for cognitively impaired patients with HIV-1 infection, but also numerous inflammatory diseases for which such antiplatelet therapies are currently lacking.
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Registered trials
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.