ArticleThe Journal of clinical investigation1997
Nitric oxide production contributes to the angiogenic properties of vascular endothelial growth factor in human endothelial cells.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 349 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
349 citing papers in PubMed, 1,180 citations in OpenAlex.
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- Potentiating anti-inflammatory and antioxidant effects in vitro: the combined action of zofenoprilat and nebivolol.Pharmacological reports : PR · 2026Article
- Effects of Pelargonium sidoides root extract on paw oedema, nitric oxide signaling, and synovial vascular changes in a rat model of adjuvant-induced arthritis.Inflammopharmacology · 2026Article
- Comprehensive analysis of the causal risk factor from hypertension associated with prognosis and therapeutic response in renal cell carcinoma by multi-omics analysis and validation.Biology direct · 2026Article
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- Significant Correlation Between Choroidal Thickness and Decrease in Choroidal Blood Flow After Switching to Brolucizumab for Refractory Neovascular Age-Related Macular Degeneration.Ophthalmology and therapy · 2026Article
- Chemical Profiles and Bioactivities of Brazilian Amazonian Solanum Species: Antioxidant, Cytotoxic, and Anti-Metastatic Properties.Chemistry & biodiversity · 2026Article
- Cyanide is an endogenous stimulator of endothelial cell proliferation, migration and differentiation.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Novel stable "sandwich" cyclodextrin inclusion of a lipophilic S-nitrosothiol for controlled delivery of nitric oxide.Materials & design · 2026Article
- Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Diet-induced obesity promotes endothelial cell desensitization to VEGF-A and permanent islet vessel dysfunction in mice.The Journal of clinical investigation · 2025Article
- L-arginine from elder human mesenchymal stem cells induces angiogenesis and enhances therapeutic effects on ischemic heart diseases.World journal of stem cells · 2025Article
- Regulatory effects of resveratrol on nitric oxide signaling in cardiovascular diseases.Pharmacological reports : PR · 2025Review
- The BCR::ABL1 tyrosine kinase inhibitors ponatinib and nilotinib differentially affect endothelial angiogenesis and signalling.Molecular and cellular biochemistry · 2025Article
- Dissecting the opposing regulatory functions of endogenous nitric oxide production in colorectal cancer initiation, adaptive immune response alterations, and ferroptosis execution.Oncology reviews · 2025Review
289 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vascular endothelial growth factor (VEGF) is a regulator of vasculogenesis and angiogenesis. To investigate the role of nitric oxide (NO) in VEGF-induced proliferation and in vitro angiogenesis, human umbilical vein endothelial cells (HUVEC) were used. VEGF stimulated the growth of HUVEC in an NO-dependent manner. In addition, VEGF promoted the NO-dependent formation of network-like structures in HUVEC cultured in three dimensional (3D) collagen gels. Exposure of cells to VEGF led to a concentration-dependent increase in cGMP levels, an indicator of NO production, that was inhibited by nitro-L-arginine methyl ester. VEGF-stimulated NO production required activation of tyrosine kinases and increases in intracellular calcium, since tyrosine kinase inhibitors and calcium chelators attenuated VEGF-induced NO release. Moreover, two chemically distinct phosphoinositide 3 kinase (PI-3K) inhibitors attenuated NO release after VEGF stimulation. In addition, HUVEC incubated with VEGF for 24 h showed an increase in the amount of endothelial NO synthase (eNOS) protein and the release of NO. In summary, both short- and long-term exposure of human EC to VEGF stimulates the release of biologically active NO. While long-term exposure increases eNOS protein levels, short-term stimulation with VEGF promotes NO release through mechanisms involving tyrosine and PI-3K kinases, suggesting that NO mediates aspects of VEGF signaling required for EC proliferation and organization in vitro.
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What OpenQuestion holds
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.