ArticleAmerican journal of physiology. Renal physiology2012
HIV-induced kidney cell injury: role of ROS-induced downregulated vitamin D receptor.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- APOL1 Modulates Renin-Angiotensin System.Biomolecules · 2024Article
- ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies.Current issues in molecular biology · 2024Review
- Piscine Vitamin D Receptors Vdra/Vdrb in the Absence of Vitamin D Are Utilized by Grass Carp Reovirus for Promoting Viral Replication.Microbiology spectrum · 2023Article
- Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D.Antioxidants (Basel, Switzerland) · 2020Review
- Hypertension and Metabolic Syndrome in Persons with HIV.Current hypertension reports · 2020Review
- Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases.Current medicinal chemistry · 2018Review
- Hedgehog pathway plays a vital role in HIV-induced epithelial-mesenchymal transition of podocyte.Experimental cell research · 2017Article
- Vitamin D receptor deficit induces activation of renin angiotensin system via SIRT1 modulation in podocytes.Experimental and molecular pathology · 2017Article
- Human cytomegalovirus infection downregulates vitamin-D receptor in mammalian cells.The Journal of steroid biochemistry and molecular biology · 2017Article
- Impact of APOL1 polymorphism and IL-1β priming in the entry and persistence of HIV-1 in human podocytes.Retrovirology · 2016Article
- Vitamin D derivatives enhance cytotoxic effects of H2O2 or cisplatin on human keratinocytes.Steroids · 2016Article
- BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells.Veterinary research · 2016Article
- HIV Promotes NLRP3 Inflammasome Complex Activation in Murine HIV-Associated Nephropathy.The American journal of pathology · 2016Article
- Epigenetic Modulation of Human Podocyte Vitamin D Receptor in HIV Milieu.Journal of molecular biology · 2015Article
- AT1R blockade in adverse milieus: role of SMRT and corepressor complexes.American journal of physiology. Renal physiology · 2015Article
- Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors.Cellular signalling · 2015Article
- Integrative analysis of differentially expressed microRNAs of pulmonary alveolar macrophages from piglets during H1N1 swine influenza A virus infection.Scientific reports · 2015Article
- Vitamin D receptor and epigenetics in HIV infection and drug abuse.Frontiers in microbiology · 2015Review
- Modulation of renin angiotensin system predominantly alters sclerotic phenotype of glomeruli in HIVAN.Histology and histopathology · 2014Article
- Renin modulates HIV replication in T cells.Journal of leukocyte biology · 2014Article
Corrections and comments
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) have been demonstrated to contribute to HIV-induced tubular cell injury. We hypothesized that HIV-induced ROS generation may be causing tubular cell injury through downregulation of vitamin D receptor (VDR) and associated downstream effects. In the present study, HIV not only downregulated tubular cell VDR expression but also inflicted DNA injury. On the other hand, EB-1089, a VDR agonist (VD), inhibited both downregulation of VDR and tubular cell DNA injury in the HIV milieu. H(2)O(2) (an O(-) donor) directly downregulated tubular cell VDR, whereas catalase, a free radical scavenger, inhibited HIV-induced downregulation of tubular cell VDR expression. HIV also stimulated the tubular cell renin-angiotensin system (RAS) through downregulation of VDR. Because losartan (an ANG II blolcker) partially inhibited HIV-induced tubular cell ROS generation while ANG II directly stimulated tubular cell ROS generation, it appears that HIV-induced ROS production was partly contributed by the RAS activation. VD not only inhibited HIV-induced RAS activation but also attenuated tubular cell ROS generation. Tubular cells displayed double jeopardy in the HIV milieu induction of double-strand breaks and attenuated DNA repair; additionally, in the HIV milieu, tubular cells exhibited enhanced expression of phospho-p53 and associated downstream signaling. A VDR agonist and an ANG II blocker not only preserved expression of tubular cell DNA repair proteins but also inhibited induction of double-strand breaks. In in vivo studies, renal cortical sections of Tg26 mice displayed attenuated expression of VDR both in podocytes and tubular cells. In addition, renal cortical sections of Tg26 mice displayed enhanced oxidative stress-induced kidney cell DNA damage. These findings indicated that HIV-induced tubular cell downregulation of VDR contributed to the RAS activation and associated tubular cell DNA damage. However, both VD and RAS blockade provided protection against these effects of HIV.
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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.