Decorin Mimic Regulates Platelet-Derived Growth Factor and Interferon-γ Stimulation of Vascular Smooth Muscle Cells

Scott, R.; Panitch, Alyssa

doi:10.1021/bm500224f

Cited by 24 publications

(24 citation statements)

References 65 publications

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“…The binding to type I, type VI collagen and fibronectin affects collagen fibril formation and modulates the ECM rigidity and stiffness, structural properties known to influence angiogenesis [159,160,161]. As other ECM molecule, decorin modulates the activity of pro-angiogenic growth factors including VEGF, PDGF, FGF, Insulin Growth Factor (IGF) and angiopoietin by sequestering them and influencing their availability [162,163,164,165]. Decorin controls also the bioavailability of TGF-β whose release depends on the activity of different proteases involved in angiogenesis [166,167].…”

Section: Proteoglycans: Complex Functions From the Protein Core Anmentioning

confidence: 99%

Extracellular Matrix, a Hard Player in Angiogenesis

Mongiat

Andreuzzi

Tarticchio

et al. 2016

IJMS

162

133

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The extracellular matrix (ECM) is a complex network of proteins, glycoproteins, proteoglycans, and polysaccharides. Through multiple interactions with each other and the cell surface receptors, not only the ECM determines the physical and mechanical properties of the tissues, but also profoundly influences cell behavior and many physiological and pathological processes. One of the functions that have been extensively explored is its impingement on angiogenesis. The strong impact of the ECM in this context is both direct and indirect by virtue of its ability to interact and/or store several growth factors and cytokines. The aim of this review is to provide some examples of the complex molecular mechanisms that are elicited by these molecules in promoting or weakening the angiogenic processes. The scenario is intricate, since matrix remodeling often generates fragments displaying opposite effects compared to those exerted by the whole molecules. Thus, the balance will tilt towards angiogenesis or angiostasis depending on the relative expression of pro- or anti-angiogenetic molecules/fragments composing the matrix of a given tissue. One of the vital aspects of this field of research is that, for its endogenous nature, the ECM can be viewed as a reservoir to draw from for the development of new more efficacious therapies to treat angiogenesis-dependent pathologies.

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Section: Proteoglycans: Complex Functions From the Protein Core Anmentioning

confidence: 99%

Extracellular Matrix, a Hard Player in Angiogenesis

Mongiat

Andreuzzi

Tarticchio

et al. 2016

IJMS

162

133

View full text Add to dashboard Cite

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“…In addition to VEGF and TGF-β, decorin interacts with several other angiogenic growth factors, including platelet-derived growth factor (PDGF) [123,142,143], fibroblast growth factor (FGF) [93,144], insulin-like growth factor (IGF) [120,121,145], connective tissue growth factor (CTGF) [146–148], and HGF [118,149]. Furthermore, decorin influences the availability of the proangiogenic factor angiopoietin, as well [94].…”

Section: Potential Mechanism(s) For Decorin In Angiogenesismentioning

confidence: 99%

Pivotal role for decorin in angiogenesis

2015

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Angiogenesis, the formation of new blood vessels from preexisting vessels, is a highly complex process. It is regulated in a finely-tuned manner by numerous molecules including not only soluble growth factors such as vascular endothelial growth factor and several other growth factors, but also a diverse set of insoluble molecules, particularly collagenous and non-collagenous matrix constituents. In this review we have focused on the role and potential mechanisms of a multifunctional small leucine-rich proteoglycan decorin in angiogenesis. Depending on the cellular and molecular microenvironment where angiogenesis occurs, decorin can exhibit either a proangiogenic or an antiangiogenic activity. Nevertheless, in tumorigenesis-associated angiogenesis and in various inflammatory processes, particularly foreign body reactions and scarring, decorin exhibits an antiangiogenic activity, thus providing a potential basis for the development of decorin-based therapies in these pathological situations.

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“…Cytotoxins currently utilized to minimize maladaptive cell behaviour following PCI are non‐selective, and the goal for functional vascular healing should be a development of new active ingredients that promote EC growth while inhibiting unregulated SMC behaviour. Previously, we have demonstrated that DS–SILY 20 modulates SMC migration, protein synthesis, cytokine secretion and vascular injury marker production in both proliferative and quiescent SMCs (Scott et al ., ; Scott and Panitch, ). Conversely, in this study, we reveal that DS–SILY 20 supports EC proliferation and migration in vitro (Figure B, C).…”

Section: Discussionmentioning

confidence: 99%

Decorin mimic promotes endothelial cell health in endothelial monolayers and endothelial–smooth muscle co‐cultures

Scott

Ramaswamy

Park

et al. 2015

J Tissue Eng Regen Med

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Non-specific cytotoxins, including paclitaxel and sirolimus analogues, currently utilized as anti-restenotic therapeutics, affect not only smooth muscle cells (SMCs) but also neighbouring vascular endothelial cells (ECs). These drugs inhibit the formation of an intact endothelium following vessel injury, thus emphasizing the critical need for new candidate therapeutics. Utilizing our in vitro models, including EC monolayers and both hyperplastic and quiescent EC-SMC co-cultures, we investigated the ability of DS-SILY , a decorin mimic, to promote EC health. DS-SILY increased EC proliferation and migration by 1.5- and 2-fold, respectively, which corresponded to increased phosphorylation of ERK-1/2. Interestingly, IL-6 secretion and the production of both E-selectin and P-selectin were reduced in the presence of 10 μm DS-SILY , even in the presence of the potent pro-inflammatory cytokine platelet-derived growth factor (PDGF). In hyperplastic and quiescent EC-SMC co-cultures, DS-SILY treatment reduced the secretion of IFNγ, IL-1β, IL-6 and TNFα, corresponding to a 23% decrease in p38 phosphorylation. E-selectin and P-selectin expression was further reduced following DS-SILY treatment in both co-culture models. These results indicate that DS-SILY promotes EC health and that this decorin mimic could serve as a potential therapeutic to promote vessel healing following percutaneous coronary intervention (PCI). Copyright © 2015 John Wiley & Sons, Ltd.

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Decorin Mimic Regulates Platelet-Derived Growth Factor and Interferon-γ Stimulation of Vascular Smooth Muscle Cells

Cited by 24 publications

References 65 publications

Extracellular Matrix, a Hard Player in Angiogenesis

Extracellular Matrix, a Hard Player in Angiogenesis

Pivotal role for decorin in angiogenesis

Decorin mimic promotes endothelial cell health in endothelial monolayers and endothelial–smooth muscle co‐cultures

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