ArticleThe Journal of biological chemistry2012
The unfolded protein response regulates an angiogenic response by the kidney epithelium during ischemic stress.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Emerging roles of endoplasmic reticulum stress in the cellular plasticity of cancer cells.Frontiers in oncology · 2023Review
- Pro- and anti-fibrotic effects of vascular endothelial growth factor in chronic kidney diseases.Renal failure · 2022Review
- Klotho alleviates chronic intermittent hypoxia-induced genioglossus myocyte apoptosis by inhibiting endoplasmic reticulum stress.Experimental and therapeutic medicine · 2021Article
- The endoplasmic reticulum stress and the unfolded protein response in kidney disease: Implications for vascular growth factors.Journal of cellular and molecular medicine · 2020Review
- Inhibition of oxygen-sensing prolyl hydroxylases increases lipid accumulation in human primary tubular epithelial cells without inducing ER stress.Cell and tissue research · 2020Article
- tRNA fragmentation and protein translation dynamics in the course of kidney injury.RNA biology · 2018Review
- Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases.Nature reviews. Nephrology · 2017Review
- Salubrinal attenuated retinal neovascularization by inhibiting CHOP-HIF1α-VEGF pathways.Oncotarget · 2017Article
- Angiogenin Mediates Cell-Autonomous Translational Control under Endoplasmic Reticulum Stress and Attenuates Kidney Injury.Journal of the American Society of Nephrology : JASN · 2016Article
- Low glucose microenvironment of normal kidney cells stabilizes a subset of messengers involved in angiogenesis.Physiological reports · 2015Article
- Targeting the IRE1α/XBP1 and ATF6 arms of the unfolded protein response enhances VEGF blockade to prevent retinal and choroidal neovascularization.The American journal of pathology · 2013Article
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic injuries permanently affect kidney tissue and challenge cell viability, promoting inflammation and fibrogenesis. Ischemia results in nutrient deprivation, which triggers endoplasmic reticulum stress, ultimately resulting in the unfolded protein response (UPR). The aim of this study was to test whether the UPR could promote an angiogenic response independently of the HIF-1α pathway during ischemic stress in the human kidney epithelium. Glucose deprivation induced the secretion of vascular endothelial growth factor A (VEGFA), basic fibroblast growth factor (bFGF) and angiogenin (ANG) in human kidney epithelial cells independently of HIF-1α. Glucose deprivation, but not hypoxia, triggered endoplasmic reticulum stress and activated the UPR. RNA interference-mediated inhibition of the gene encoding the kinase PERK decreased VEGFA and bFGF expression, but neither gene was affected by the inhibition of IRE1α or ATF6. Furthermore, we show that the expression of angiogenin, which inhibits protein synthesis, is regulated by both IRE1α and PERK, which could constitute a complementary function of the UPR in the repression of translation. In a rat model of acute ischemic stress, we show that the UPR is activated in parallel with VEGFA, bFGF, and ANG expression and independently of HIF-1α.
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