ArticlePloS one2010
Glucocorticoid-mediated inhibition of angiogenic changes in human endothelial cells is not caused by reductions in cell proliferation or migration.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 95 citations in OpenAlex.
- GDF11 alleviates glucocorticoid-induced osteonecrosis of the femoral head by regulating angiogenesis via the PI3K-AKT-eNOS pathway.Communications biology · 2025Article
- Sex-specific effects of betamethasone on glucocorticoid and apoptotic signalling pathways in the sheep placenta.The Journal of physiology · 2025Article
- Discovery and Functional Validation of EP3 Receptor Ligands with Therapeutic Potential in Cardiovascular Disease.International journal of molecular sciences · 2025Article
- From heterogeneity to prognosis: understanding the complexity of tertiary lymphoid structures in tumors.Molecular biology reports · 2025Review
- Mechanisms of endometrial aging: lessons from natural conceptions and assisted reproductive technology cycles.Frontiers in physiology · 2024Review
- Vascular and Collagen Target: A Rational Approach to Hypertrophic Scar Management.Advances in wound care · 2023Review
- The Effects of Abscisic Acid on Angiogenesis in Both ex vivo and in vivo Assays.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Glucocorticoid therapy in respiratory illness: bench to bedside.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022Review
- Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022Review
- Hormone regulation of thrombospondin-1 mRNA in porcine granulosa cells in vitro.Animal reproduction science · 2022Article
- Selective Serotonin Reuptake Inhibitor Promotes Bone-Tendon Interface Healing in a Rotator Cuff Tear Rat Model.Tissue engineering and regenerative medicine · 2022Article
- Uterine bleeding: how understanding endometrial physiology underpins menstrual health.Nature reviews. Endocrinology · 2022Review
- An in-vivo study of photobiomodulation using 403 nm and 649 nm diode lasers for molar tooth extraction wound healing in wistar rats.Odontology · 2022Article
- Lymphatic Vessel Regression and Its Therapeutic Applications: Learning From Principles of Blood Vessel Regression.Frontiers in physiology · 2022Review
- Role of Endothelial Glucocorticoid Receptor in the Pathogenesis of Kidney Diseases.International journal of molecular sciences · 2021Review
- Glucocorticoid therapy in assisted reproduction.Clinical and experimental reproductive medicine · 2021Article
- Glucocorticoid-induced osteonecrosis in systemic lupus erythematosus patients.Clinical and translational medicine · 2021Review
- Dexamethasone Inhibits the Pro-Angiogenic Potential of Primary Human Myoblasts.International journal of molecular sciences · 2021Article
- Review
- Heterogeneity and Dynamics of Vasculature in the Endocrine System During Aging and Disease.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlucocorticoid-mediated inhibition of angiogenesis is important in physiology, pathophysiology and therapy. However, the mechanisms through which glucocorticoids inhibit growth of new blood vessels have not been established. This study addresses the hypothesis that physiological levels of glucocorticoids inhibit angiogenesis by directly preventing tube formation by endothelial cells. METHODOLOGY/PRINCIPAL
findingsCultured human umbilical vein (HUVEC) and aortic (HAoEC) endothelial cells were used to determine the influence of glucocorticoids on tube-like structure (TLS) formation, and on cellular proliferation (5-bromo-2'-deoxyuridine (BrdU) incorporation), viability (ATP production) and migration (Boyden chambers). Dexamethasone or cortisol (at physiological concentrations) inhibited both basal and prostaglandin F(2α) (PGF(2α))-induced and vascular endothelial growth factor (VEGF) stimulated TLS formation in endothelial cells (ECs) cultured on Matrigel, effects which were blocked with the glucocorticoid receptor antagonist RU38486. Glucocorticoids had no effect on EC viability, migration or proliferation. Time-lapse imaging showed that cortisol blocked VEGF-stimulated cytoskeletal reorganisation and initialisation of tube formation. Real time PCR suggested that increased expression of thrombospodin-1 contributed to glucocorticoid-mediated inhibition of TLS formation. CONCLUSIONS/SIGNIFICANCE: We conclude that glucocorticoids interact directly with glucocorticoid receptors on vascular ECs to inhibit TLS formation. This action, which was conserved in ECs from two distinct vascular territories, was due to alterations in cell morphology rather than inhibition of EC viability, migration or proliferation and may be mediated in part by induction of thrombospodin-1. These findings provide important insights into the anti-angiogenic action of endogenous glucocorticoids in health and disease.
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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.