Angiogenesis

Folkman, Judah

doi:10.1146/annurev.med.57.121304.131306

Cited by 1,211 publications

(964 citation statements)

References 90 publications

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“…Although endothelial cells are not professional phagocytes, their migration is an essential contributor to angiogenesis, which is important for tissue healing, development, and cancer progression [70]. Many different types of endothelial cells exhibit a chemotactic response to extracellular nucleotides; the P2Y 1 receptor has been implicated as a mediator of this process [71,72].…”

Section: Endothelial Cellsmentioning

confidence: 99%

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

Corriden

Insel

2012

Purinergic Signalling

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The directional movement of cells can be regulated by ATP, certain other nucleotides (e.g., ADP, UTP), and adenosine. Such regulation occurs for cells that are "professional phagocytes" (e.g., neutrophils, macrophages, certain lymphocytes, and microglia) and that undergo directional migration and subsequent phagocytosis. Numerous other cell types (e.g., fibroblasts, endothelial cells, neurons, and keratinocytes) also change motility and migration in response to ATP, other nucleotides, and adenosine. In this article, we review how nucleotides and adenosine modulate chemotaxis and motility and highlight the importance of nucleotide-and adenosine-regulated cell migration in several cell types: neutrophils, microglia, endothelial cells, and cancer cells. We also discuss difficulties in conducting experiments and drawing conclusions regarding the ability of nucleotides and adenosine to modulate the migration of professional and non-professional phagocytes.

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Section: Endothelial Cellsmentioning

confidence: 99%

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

Corriden

Insel

2012

Purinergic Signalling

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“…FGF-2, along with stimulating critical steps in endothelial cell tube formation, further enhances extracellular matrix degradation through production of urokinase plasminogen activator and matrix metalloproteinases (Presta et al 2005). As the matrix is degraded, extracellular matrix protein fragments inhibit angiogenesis (Kalluri 2003;Folkman 2006). The pro-and anti-angiogenic balance within the extracellular matrix keeps physiological angiogenesis focal and time-limited (Folkman 2007).…”

Section: Introductionmentioning

confidence: 99%

Vascular growth factor binding kinetics to the endothelial cell basement membrane, with a kinetics-based correction for substrate binding

Clyne

Edelman

2009

Cytotechnology

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Vascular growth factors, including vascular endothelial growth factor and fibroblast growth factor-2, bind to heparan sulfate proteoglycans in the basement membrane. While this binding, storage, and release system provides a critical model for controlled drug release devices, basement membrane-growth factor binding kinetics have not been fully established. We modified endothelial cell-growth factor binding kinetics protocols for the basement membrane. The basement membrane showed low affinity for fibroblast growth factor-2 (K d = 185.8 nM), with a slow off rate (k off = 0.00338 min -1 ). However, results were confounded by growth factor binding to tissue culture polystyrene in a manner strikingly similar to basement membrane. Since substrate binding could not be blocked, a binding kinetics based correction technique was developed to account for polystyrene growth factor binding. This method was validated by conducting binding kinetics experiments on bacteriologic plates that exhibit little growth factor binding. This novel method will improve our understanding of cell and protein interaction with the basement membrane in health and disease. They can also further be applied to develop biomimetic drug delivery systems.

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“…Angiogenesis is the process of new vessel formation from an established vascular plexus (Folkman, 2006). Under nonpathological conditions, it is a tightly regulated process representing a balance between stimulating and inhibiting factors (Ferrara and Kerbel, 2005).…”

Section: Introductionmentioning

confidence: 99%

Modulation of angiogenesis by dithiolethione‐modified NSAIDs and valproic acid

Isenberg

Jia

Field

et al. 2007

British J Pharmacology

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Background and purpose: Angiogenesis involves multiple signaling pathways that must be considered when developing agents to modulate pathological angiogenesis. Because both cyclooxygenase inhibitors and dithioles have demonstrated antiangiogenic properties, we investigated the activities of a new class of anti-inflammatory drugs containing dithiolethione moieties (S-NSAIDs) and S-valproate. Experimental approach: Anti-angiogenic activities of S-NSAIDS, S-valproate, and the respective parent compounds were assessed using umbilical vein endothelial cells, muscle and tumor tissue explant angiogenesis assays, and developmental angiogenesis in Fli:EGFP transgenic zebrafish embryos. Key results: Dithiolethione derivatives of diclofenac, valproate, and sulindac inhibited endothelial cell proliferation and induced Ser 78 phosphorylation of hsp27, a known molecular target of anti-angiogenic signaling. The parent drugs lacked this activity, but dithiolethiones were active at comparable concentrations. Although dithiolethiones can potentially release hydrogen sulphide, NaSH did not reproduce some activities of the S-NSAIDs, indicating that the dithioles regulate angiogenesis through mechanisms other than release of H 2 S. In contrast to the parent drugs, S-NSAIDs, S-valproate, NaSH, and dithiolethiones were potent inhibitors of angiogenic responses in muscle and HT29 tumor explants assessed by 3-dimensional collagen matrix assays. Dithiolethiones and valproic acid were also potent inhibitors of developmental angiogenesis in zebrafish embryos, but the S-NSAIDs, remarkably, lacked this activity. Conclusions and implication: S-NSAIDs and S-valproate have potent anti-angiogenic activities mediated by their dithiole moieties. The novel properties of S-NSAIDs and S-valproate to inhibit pathological versus developmental angiogenesis suggest that these agents may have a role in cancer treatment.

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Angiogenesis

Cited by 1,211 publications

References 90 publications

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

New insights regarding the regulation of chemotaxis by nucleotides, adenosine, and their receptors

Vascular growth factor binding kinetics to the endothelial cell basement membrane, with a kinetics-based correction for substrate binding

Modulation of angiogenesis by dithiolethione‐modified NSAIDs and valproic acid

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