ArticleJournal of the American Society of Nephrology : JASN2008
Endotoxin mediates recruitment of RNA polymerase II to target genes in acute renal failure.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- Histone methylation of kidney disease: fact or fantasy?Renal failure · 2025Review
- Epigenetic memories induced by hypoxia in AKI-to-CKD transition.Clinical and experimental nephrology · 2025Review
- Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury.Frontiers in physiology · 2024Review
- Sepsis-associated acute kidney injury: consensus report of the 28th Acute Disease Quality Initiative workgroup.Nature reviews. Nephrology · 2023Review
- Immunometabolic rewiring of tubular epithelial cells in kidney disease.Nature reviews. Nephrology · 2022Review
- Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Protein Methylation in Diabetic Kidney Disease.Frontiers in medicine · 2022Review
- Nephrotoxicity of perfluorooctane sulfonate (PFOS)-effect on transcription and epigenetic factors.Environmental epigenetics · 2022Article
- Metabolic Reprogramming and Host Tolerance: A Novel Concept to Understand Sepsis-Associated AKI.Journal of clinical medicine · 2021Review
- Pathophysiological Mechanisms by which Heat Stress Potentially Induces Kidney Inflammation and Chronic Kidney Disease in Sugarcane Workers.Nutrients · 2020Article
- The Contribution of Histone Crotonylation to Tissue Health and Disease: Focus on Kidney Health.Frontiers in pharmacology · 2020Review
- Renal tubular cell spliced X-box binding protein 1 (Xbp1s) has a unique role in sepsis-induced acute kidney injury and inflammation.Kidney international · 2019Article
- Epigenetic regulation in AKI and kidney repair: mechanisms and therapeutic implications.Nature reviews. Nephrology · 2019Review
- Distinct patterns of transcriptional and epigenetic alterations characterize acute and chronic kidney injury.Scientific reports · 2018Article
- Down-regulation of GRP78 alleviates lipopolysaccharide-induced acute kidney injury.International urology and nephrology · 2018Article
- Mechanisms Underlying Increased TIMP2 and IGFBP7 Urinary Excretion in Experimental AKI.Journal of the American Society of Nephrology : JASN · 2018Article
- Methylation-Demethylation Dynamics: Implications of Changes in Acute Kidney Injury.Analytical cellular pathology (Amsterdam) · 2018Review
- Regulation of the ubiquitylation and deubiquitylation of CREB-binding protein modulates histone acetylation and lung inflammation.Science signaling · 2017Article
- The exciting "bench to bedside" journey of cell therapies for acute kidney injury and renal transplantation.Journal of nephrology · 2017Review
- Metabolic reprogramming and tolerance during sepsis-induced AKI.Nature reviews. Nephrology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Acute renal failure (ARF) sensitizes the kidney to endotoxin (LPS)-driven production of cytokines and chemokines. This study assessed whether this LPS hyperresponsiveness exists at the genomic level. Three heterogeneous mouse models of ARF were studied: Maleate nephrotoxicity, unilateral ureteral obstruction, and LPS preconditioning. In all cases, LPS was injected approximately 18 h after injury was induced, and over the next 0 to 90 min, RNA polymerase II recruitment to the genome at three LPS-responsive genes (TNF-alpha, monocyte chemoattractant-1 [MCP-1], and heme oxygenase-1 [HO-1]) was assessed by chromatin immunoprecipitation. LPS hyperresponsiveness was noted in each model, measured by exaggerated increases in TNF-alpha and MCP-1 mRNA (approximately two to 10 times higher than LPS-injected controls). Corresponding increases in the recruitment of RNA polymerase II to the TNF-alpha and MCP-1 genes were observed, and increased trimethylation of histone 3 lysine 4 (H3K4m3) at these sites may have played a role in this recruitment. Conversely, recruitment of RNA polymerase II to the HO-1 gene was suppressed ("tolerance"), and no increase in H3K4m3 was observed at HO-1 exons. The ARF-induced changes in mRNA did not correlate with mRNA stability, suggesting the mechanistic importance of RNA polymerase II-mediated transcriptional events. In conclusion, LPS hyperresponsiveness after ARF is likely mediated at the genomic level, possibly by H3K4m3.
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Registered trials
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