ArticleAmerican journal of physiology. Renal physiology2008
p53 regulates renal expression of HIF-1{alpha} and pVHL under physiological conditions and after ischemia-reperfusion injury.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Analysis of the potential ferroptosis mechanism and multitemporal expression change of central ferroptosis-related genes in cardiac ischemia-reperfusion injury.Frontiers in physiology · 2022Article
- HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury.Redox biology · 2020Article
- p53-cyclophilin D mediates renal tubular cell apoptosis in ischemia-reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2019Article
- Novel roles for mucin 1 in the kidney.Current opinion in nephrology and hypertension · 2017Review
- Loss of PIG3 increases HIF-1α level by promoting protein synthesis via mTOR pathway in renal cell carcinoma cells.Oncotarget · 2016Article
- Novel application of complementary imaging techniques to examine in vivo glucose metabolism in the kidney.American journal of physiology. Renal physiology · 2016Article
- C5a inhibitor protects against ischemia/reperfusion injury in rat small intestine.Microbiology and immunology · 2016Article
- Muc1 is protective during kidney ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2015Article
- Increase of miR-199a-5p by protoporphyrin IX, a photocatalyzer, directly inhibits E2F3, sensitizing mesenchymal tumor cells to anti-cancer agents.Oncotarget · 2015Article
- TIGAR regulates glycolysis in ischemic kidney proximal tubules.American journal of physiology. Renal physiology · 2015Article
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- The p53 inhibitor pifithrin-α can stimulate fibrosis in a rat model of ischemic acute kidney injury.American journal of physiology. Renal physiology · 2012Article
- Impaired wound healing in hypoxic renal tubular cells: roles of hypoxia-inducible factor-1 and glycogen synthase kinase 3β/β-catenin signaling.The Journal of pharmacology and experimental therapeutics · 2012Article
- Transcriptome analysis of renal ischemia/reperfusion injury and its modulation by ischemic pre-conditioning or hemin treatment.PloS one · 2012Article
- Pathogenesis of acute kidney injury: foundation for clinical practice.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2011Review
- Reciprocal influence of the p53 and the hypoxic pathways.Cell death & disease · 2011Review
- Approaches to the Management of Acute Kidney Injury in Children.Recent patents on biomarkers · 2011Article
- Trauma hemorrhagic shock-induced lung injury involves a gut-lymph-induced TLR4 pathway in mice.PloS one · 2011Article
- HIF-1 mediates pathogenic inflammatory responses to intestinal ischemia-reperfusion injury.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
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9 authors at 2 institutions in 1 country.
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Abstract
Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI) and is characterized by widespread tubular and microvascular damage. The tumor suppressor p53 is upregulated after IRI and contributes to renal injury in part by promoting apoptosis. Acute, short-term inhibition of p53 with pifithrin-alpha conveys significant protection after IRI. The hypoxia-inducible factor-1 (HIF-1) pathway is also activated after IRI and has opposing effects to those promoted by p53. The balance between the HIF-1 and p53 responses can determine the outcome of IRI. In this manuscript, we investigate whether p53 regulates the HIF-1 pathway in a rodent model of IRI. HIF-1alpha is principally expressed in the collecting tubules (CT) and thick ascending limbs (TAL) under physiological conditions. However, inhibition of p53 with pifithrin-alpha increases the faint expression of HIF-1alpha in proximal tubules (PT) under physiological conditions. Twenty-four hours after IRI, HIF-1alpha expression is decreased in both CT and TAL. HIF-1alpha expression in the PT is not significantly altered after IRI. Acute inhibition of p53 significantly increases HIF-1alpha expression in the PT after IRI. Additionally, pifithrin-alpha prevents the IRI-induced decrease in HIF-1alpha in the CT and TAL. Parallel changes are observed in the HIF-1alpha transcriptive target, carbonic anhydrase-9. Finally, inhibition of p53 prevents the dramatic changes in Von Hippel-Lindau protein morphology and expression after IRI. We conclude that activation of p53 after IRI mitigates the concomitant activation of the protective HIF-1 pathway. Modulating the interactions between the p53 and HIF-1 pathway can provide novel options in the treatment of AKI.
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