ArticleThe American journal of pathology2002
Human immunodeficiency virus-1 tat induces hyperproliferation and dysregulation of renal glomerular epithelial cells.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
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- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Proteomic Changes Induced by the Immunosuppressant Everolimus in Human Podocytes.International journal of molecular sciences · 2024Article
- Rational design, synthesis and structural characterization of peptides and peptidomimetics to target Hsp90/Cdc37 interaction for treating hepatocellular carcinoma.Computational and structural biotechnology journal · 2023Article
- The HDL mimetic CER-001 remodels plasma lipoproteins and reduces kidney lipid deposits in inherited lecithin:cholesterol acyltransferase deficiency.Journal of internal medicine · 2022Article
- Mesenchymal Stromal Cell-Derived Extracellular Vesicles Pass through the Filtration Barrier and Protect Podocytes in a 3D Glomerular Model under Continuous Perfusion.Tissue engineering and regenerative medicine · 2021Article
- Article
- Mechanisms of Proteinuria in HIV.Frontiers in medicine · 2021Review
- Hantavirus Induced Kidney Disease.Frontiers in medicine · 2021Review
- HIV-associated nephropathy: Protocol and rationale for an exploratory genotype-phenotype study in a sub-Saharan African population.PloS one · 2021Article
- An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.Disease models & mechanisms · 2020Article
- Acute Tubular Injury is Associated With Severe Traumatic Brain Injury: in Vitro Study on Human Tubular Epithelial Cells.Scientific reports · 2019Observational
- Role of Podocyte Injury in Glomerulosclerosis.Advances in experimental medicine and biology · 2019Review
- Effect of HIV-1 Tat on the formation of the mitotic spindle by interaction with ribosomal protein S3.Scientific reports · 2018Article
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- Src family kinases in chronic kidney disease.American journal of physiology. Renal physiology · 2017Review
- Article
- Podocyte Number in Children and Adults: Associations with Glomerular Size and Numbers of Other Glomerular Resident Cells.Journal of the American Society of Nephrology : JASN · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus-associated nephropathy (HIVAN) is etiologically related to the viral infection, but the mechanisms of virus-induced renal injury remain undetermined. Peculiar histopathological features of HIVAN are the enhanced proliferation and the loss of differentiation markers of glomerular epithelial cells (podocytes). We found that podocytes were not permissive to HIV-1 replication. In this study we investigated the effects of the HIV-1 regulatory protein Tat on primary cultures and on a continuous line of podocytes. Our results demonstrated that Tat induced hyperproliferation of these cells in a dose-dependent manner. This activity was primarily mediated by the basic domain of the viral protein. Proteoglycans were required for this phenomenon because Tat-induced increase of podocyte growth was significantly impaired by inhibition of proteoglycan synthesis with beta-D-xyloside. In podocyte cultures Tat promoted both the transcription and the release of basic fibroblast growth factor, which contributed to the enhanced cell proliferation. Moreover, Tat deregulated the podocyte phenotype causing down-regulation of maturity markers such as WT-1 and synaptopodin, alteration of cytoarchitecture, and impairment of permselectivity. Together, these results demonstrate that the interaction of extracellular Tat with podocytes can induce alterations that mimic the pathological changes of podocytes detected in HIVAN.
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