ArticleThe Journal of clinical investigation1995
Endothelial cell tolerance to hypoxia. Potential role of purine nucleotide phosphates.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 54 citations in OpenAlex.
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- Does remote ischaemic conditioning reduce inflammation? A focus on innate immunity and cytokine response.Basic research in cardiology · 2021Review
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- BDNF Overexpression Enhances the Preconditioning Effect of Brief Episodes of Hypoxia, Promoting Survival of GABAergic Neurons.Neuroscience bulletin · 2020Article
- Cell-specific metabolomic responses to injury: novel insights into blood-brain barrier modulation.Scientific reports · 2020Article
- Effect of short-term ischemia on microcirculation and wound healing of adipocutaneous flaps in the rat.Acta cirurgica brasileira · 2020Article
- Metabolic signatures of Besnoitia besnoiti-infected endothelial host cells and blockage of key metabolic pathways indicate high glycolytic and glutaminolytic needs of the parasite.Parasitology research · 2016Article
- Autocrine VEGF Isoforms Differentially Regulate Endothelial Cell Behavior.Frontiers in cell and developmental biology · 2016Article
- Dose-dependent effects of allopurinol on human foreskin fibroblast cells and human umbilical vein endothelial cells under hypoxia.PloS one · 2015Article
- Endothelial cell metabolism and implications for cancer therapy.British journal of cancer · 2012Review
- Low intracellular ATP levels exacerbate carcinogen-induced inflammatory stress response and inhibit in vitro tubulogenesis in human brain endothelial cells.Journal of inflammation research · 2011Article
- MicroRNA-210 controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2.Cell metabolism · 2009Article
- Extensive deendothelialization and thrombogenicity in routinely prepared vein grafts for coronary bypass operations: facts and remedy.International journal of clinical and experimental medicine · 2009Article
- Mitochondria as signaling organelles in the vascular endothelium.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Therapeutic targets for hypoxia-elicited pathways.Pharmaceutical research · 1999Review
- Hypoxia enhances stimulus-dependent induction of E-selectin on aortic endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability of cells to tolerate hypoxia is critical to their survival, but varies greatly among different cell types. Despite alterations in many cellular responses during hypoxic exposure, pulmonary arterial endothelial cells (PAEC) retain their viability and cellular integrity. Under similar experimental conditions, other cell types, exemplified by renal tubular epithelial cells, are extremely hypoxia sensitive and are rapidly and irreversibly damaged. To investigate potential mechanisms by which PAEC maintain cellular and functional integrity under these conditions, we compared the turnover of adenine and guanine nucleotides in hypoxia tolerant PAEC and in hypoxia-sensitive renal tubular endothelial cells under various hypoxic conditions. Under several different hypoxic conditions, hypoxia-tolerant PAEC maintained or actually increased ATP levels and the percentage of these nucleotides found in the high energy phosphates, ATP and GTP. In contrast, in hypoxia-sensitive renal tubular endothelial cells, the same high energy phosphates were rapidly depleted. Yet, in both cell types, there were minor alterations in the uptake of the precusor nucleotide and its incorporation into the appropriate purine nucleotide phosphates and marked decreases in ATPase and GTPase activity. This maintenance of high energy phosphates in hypoxic PAEC suggests that there exists tight regulation of ATP and GTP turnover in these cells and that preservation of these nucleotides may contribute to the tolerance of PAEC to acute and chronic hypoxia.
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Registered trials
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.