ArticleAmerican journal of physiology. Renal physiology2006
Persistent NF-kappaB activation in renal epithelial cells in a mouse model of HIV-associated nephropathy.
Article in American journal of physiology. Renal physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Suppression of HIV-1 replication by antiretroviral therapy improves renal function in persons with low CD4 cell counts and chronic kidney disease.AIDS (London, England) · 2008Trial
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Meprin β regulates osteopontin-signaling in ischemia/reperfusion-induced kidney injury.BMC nephrology · 2025Article
- Similarities and Differences between COVID-19-Associated Nephropathy and HIV-Associated Nephropathy.Kidney diseases (Basel, Switzerland) · 2022Review
- 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 Role of Glucocorticoid Receptors in Podocytes and Nephrotic Syndrome.Nuclear receptor research · 2018Article
- Tubular cell phenotype in HIV-associated nephropathy: role of phospholipid lysophosphatidic acid.Experimental and molecular pathology · 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
- Expression of HIV transgene aggravates kidney injury in diabetic mice.Kidney international · 2013Article
- Down-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition.The Journal of biological chemistry · 2012Article
- TM4SF10 and ADAP interaction in podocytes: role in Fyn activity and nephrin phosphorylation.American journal of physiology. Cell physiology · 2011Article
- Advances in our understanding of the pathogenesis of HIV-1 associated nephropathy in children.Future virology · 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
- TNFR2 interposes the proliferative and NF-κB-mediated inflammatory response by podocytes to TNF-α.Laboratory investigation; a journal of technical methods and pathology · 2011Article
- Biophysical properties of normal and diseased renal glomeruli.American journal of physiology. Cell physiology · 2011Article
- Renal HIV expression is unaffected by serum LPS levels in an HIV transgenic mouse model of LPS induced kidney injury.PloS one · 2011Article
- The ubiquitin-like protein FAT10 mediates NF-kappaB activation.Journal of the American Society of Nephrology : JASN · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is caused, in part, by direct infection of kidney epithelial cells by HIV-1. In the spectrum of pathogenic host-virus interactions, abnormal activation or suppression of host transcription factors is common. NF-kappaB is a necessary host transcription factor for HIV-1 gene expression, and it has been shown that NF-kappaB activity is dysregulated in many naturally infected cell types. We show here that renal glomerular epithelial cells (podocytes) expressing the HIV-1 genome, similar to infected immune cells, also have a dysregulated and persistent activation of NF-kappaB. Although podocytes produce p50, p52, RelA, RelB, and c-Rel, electrophoretic mobility shift assays and immunocytochemistry showed a predominant nuclear accumulation of p50/RelA-containing NF-kappaB dimers in HIV-1-expressing podocytes compared with normal. In addition, the expression level of a transfected NF-kappaB reporter plasmid was significantly higher in HIVAN podocytes. The mechanism of NF-kappaB activation involved increased phosphorylation of IkappaBalpha, resulting in an enhanced turnover of the IkappaBalpha protein. There was no evidence for regulation by IkappaBbeta or the alternate pathway of NF-kappaB activation. Altered activation of this key host transcription factor likely plays a role in the well-described cellular phenotypic changes observed in HIVAN, such as proliferation. Studies with inhibitors of proliferation and NF-kappaB suggest that NF-kappaB activation may contribute to the proliferative mechanism in HIVAN. In addition, because NF-kappaB regulates many aspects of inflammation, this dysregulation may also contribute to disease severity and progression through regulation of proinflammatory processes in the kidney microenvironment.
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