ArticleThe American journal of pathology1997
Nitric oxide synthase inhibitors attenuate transforming-growth-factor-beta 1-stimulated capillary organization in vitro.
Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
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Who cites it
22 citing papers in PubMed, 119 citations in OpenAlex.
- Nitric oxide synthase and reduced arterial tone contribute to arteriovenous malformation.Science advances · 2023Article
- Current and emerging therapies for corneal neovascularization.The ocular surface · 2018Review
- Effect of leg immersion in mild warm carbonated water on skin and muscle blood flow.Physiological reports · 2018Article
- Enhancing amplification of late-outgrowth endothelial cells by bilobalide.Journal of cellular and molecular medicine · 2018Article
- The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Regulation and role of endogenously produced hydrogen sulfide in angiogenesis.Pharmacological research · 2016Review
- Emerging role of PKA/eNOS pathway in therapeutic angiogenesis for ischaemic tissue diseases.Cardiovascular research · 2012Review
- Endothelial dysfunction and diabetes: effects on angiogenesis, vascular remodeling, and wound healing.International journal of vascular medicine · 2012Article
- Therapeutic angiogenesis in diabetes and hypercholesterolemia: influence of oxidative stress.Antioxidants & redox signaling · 2009Review
- Cyclic GMP signaling in cardiovascular pathophysiology and therapeutics.Pharmacology & therapeutics · 2009Review
- Optimization of adenovirus-mediated endothelial nitric oxide synthase delivery in rat hindlimb ischemia.Gene therapy · 2005Article
- Expression of endothelial nitric oxide synthase in the vascular wall during arteriogenesis.Molecular and cellular biochemistry · 2004Article
- Growth factor activation in myocardial vascularization: therapeutic implications.Molecular and cellular biochemistry · 2004Review
- 17-beta-oestradiol-induced vasorelaxation in vitro is mediated by eNOS through hsp90 and akt/pkb dependent mechanism.British journal of pharmacology · 2002Article
- Nitric oxide is an essential negative regulator of cell proliferation in Xenopus brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Specific pattern of p53 phosphorylation during nitric oxide-induced cell cycle arrest.Oncogene · 2000Article
- Endogenously produced nitric oxide inhibits endothelial cell growth as demonstrated using novel antisense cell lines.British journal of pharmacology · 2000Article
- Nitric oxide synthase expression, enzyme activity and NO production during angiogenesis in the chick chorioallantoic membrane.British journal of pharmacology · 2000Article
- Nitric oxide synthase inhibition by N(G)-nitro-L-arginine methyl ester inhibits tumor-induced angiogenesis in mammary tumors.The American journal of pathology · 1999Article
- Nitric oxide synthase modulates angiogenesis in response to tissue ischemia.The Journal of clinical investigation · 1998Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Angiogenesis is a complex process involving endothelial cell (EC) proliferation, migration, differentiation, and organization into patent capillary networks. Nitric oxide (NO), an EC mediator, has been reported to be antigenic as well as proangiogenic in different models of in vivo angiogenesis. Our aim was to investigate the role of NO in capillary organization using rat microvascular ECs (RFCs) grown in three-dimensional (3D) collagen gels. RFCs placed in 3D cultures exhibited extensive tube formation in the presence of transforming growth factor-beta 1. Addition of the NO synthase (NOS) inhibitors L-nitro-arginine methylester (L-NAME, 1 mmol/L) or L-monomethyl-nitro-l-arginine (1 mmol/L) inhibited tube formation and the accumulation of nitrite in the media by approximately 50%. Incubation of the 3D cultures with excess L-arginine reversed the inhibitory effect of L-NAME on tube formation. In contrast to the results obtained in 3D cultures, inhibition of NO synthesis by L-NAME did not influence RFC proliferation in two-dimensional (2D) cultures or antagonize the ability of transforming growth factor-beta 1 to suppress EC proliferation in 2D cultures. Reverse transcriptase-polymerase chain reaction revealed the constitutive expression of all three NOS isoforms, neuronal, inducible, and endothelial NOSs, in 2D and 3D cultures. Moreover, Western blot analysis demonstrated the presence of immunoreactive protein for all NOS isoforms in 3D cultures of RFCs. In addition, in the face of NOS blockade, co-treatment with the NO donor sodium nitroprusside or the stable analog of cGMP, 8-bromo-cGMP, restored capillary tube formation. Thus, the autocrine production of NO and the activation of soluble guanylate cyclase are necessary events in the process of differentiation and in vitro capillary tube organization of RFCs.
Indexed as
Identifiers
9137106PMC1858220W1851900372What 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.