ArticleJournal of the American Society of Nephrology : JASN2005
NF-kappaB regulates Fas-mediated apoptosis in HIV-associated nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- An Update on Viral Infection-Associated Collapsing Glomerulopathy.Advances in kidney disease and health · 2024Review
- NEF-Induced HIV-Associated Nephropathy Through HCK/LYN Tyrosine Kinases.The American journal of pathology · 2023Article
- Molecular pathways associated with oxidative stress and their potential applications in radiotherapy (Review).International journal of molecular medicine · 2022Review
- Hantavirus Induced Kidney Disease.Frontiers in medicine · 2021Review
- Notch4 activation aggravates NF-κB-mediated inflammation in HIV-1-associated nephropathy.Disease models & mechanisms · 2019Article
- The HIV protease inhibitor darunavir prevents kidney injury via HIV-independent mechanisms.Scientific reports · 2019Article
- The Human FSGS-CausingJournal of the American Society of Nephrology : JASN · 2018Article
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- The Role of Glucocorticoid Receptors in Podocytes and Nephrotic Syndrome.Nuclear receptor research · 2018Article
- Krüppel-like factor 6 regulates mitochondrial function in the kidney.The Journal of clinical investigation · 2015Article
- HIV-associated nephropathies: epidemiology, pathology, mechanisms and treatment.Nature reviews. Nephrology · 2015Review
- α-Actinin 4 potentiates nuclear factor κ-light-chain-enhancer of activated B-cell (NF-κB) activity in podocytes independent of its cytoplasmic actin binding function.The Journal of biological chemistry · 2015Article
- Review
- mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN.American journal of physiology. Renal physiology · 2013Article
- Down-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition.The Journal of biological chemistry · 2012Article
- Kruppel-like factor 15 (KLF15) is a key regulator of podocyte differentiation.The Journal of biological chemistry · 2012Article
- Renal issues in HIV infection.Current HIV/AIDS reports · 2011Review
- Identification of the nephropathy-susceptibility locus HIVAN4.Journal of the American Society of Nephrology : JASN · 2011Article
- The molecular pathogenesis of HIV-1 associated nephropathy: recent advances.Journal of molecular medicine (Berlin, Germany) · 2011Review
- HIV-associated nephropathy: pathogenesis.Current opinion in nephrology and hypertension · 2011Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Renal parenchymal injury in HIV-associated nephropathy (HIVAN) is characterized by epithelial proliferation, dedifferentiation, and apoptosis along the entire length of the nephron. Although apoptotic cell death in HIVAN has been well documented, the mechanism for HIV-induced apoptosis is poorly understood. Whether the epithelial apoptosis in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here. In human HIVAN and HIV-1 transgenic mouse kidney specimens, the expression of Fas receptor and ligand proteins were markedly upregulated on epithelium in diseased glomerular and tubulointerstitial compartments when compared with normal. Podocyte cell lines that were derived from HIV-1 transgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas ligand by semiquantitative reverse transcription-PCR and Western blotting. In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 activity and apoptosis in both normal and HIVAN podocytes. Because constitutive NF-kappaB activity has been demonstrated in HIVAN epithelia, evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought. With the use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN podocytes, indicating increased transcriptional activity. In addition, chromatin immunoprecipitation assays were performed to demonstrate that p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF-kappaB with a peptide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes. These results suggest that NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium.
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