Is Syndecan-2 a Key Angiogenic Element?

Noguer, Oriol; Reina, Manuel

doi:10.1100/tsw.2009.89

Cited by 6 publications

(4 citation statements)

References 38 publications

(39 reference statements)

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“…On the other hand, SDC-4 is implicated in processes involving vascular defects in fetal placental labyrinth and poor angiogenic response in postnatal wound healing ( 14 , 24 ). We should note at this point that SDC-2 mutants have not been reported so far, but it has been established that SDC-2 plays an important function in the angiogenic process ( 25 ). Moreover, Noguer et al showed that SDC-2 impairs angiogenesis in human microvascular endothelial cells ( 26 ).…”

Section: Tumor Microenvironment and Hspgsmentioning

confidence: 91%

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

et al. 2014

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Extracellular matrix (ECM) components form a dynamic network of key importance for cell function and properties. Key macromolecules in this interplay are syndecans (SDCs), a family of transmembrane heparan sulfate proteoglycans (HSPGs). Specifically, heparan sulfate (HS) chains with their different sulfation pattern have the ability to interact with growth factors and their receptors in tumor microenvironment, promoting the activation of different signaling cascades that regulate tumor cell behavior. The affinity of HS chains with ligands is altered during malignant conditions because of the modification of chain sequence/sulfation pattern. Furthermore, matrix degradation enzymes derived from the tumor itself or the tumor microenvironment, like heparanase and matrix metalloproteinases, ADAM as well as ADAMTS are involved in the cleavage of SDCs ectodomain at the HS and protein core level, respectively. Such released soluble SDCs “shed SDCs” in the ECM interact in an autocrine or paracrine manner with the tumor or/and stromal cells. Shed SDCs, upon binding to several matrix effectors, such as growth factors, chemokines, and cytokines, have the ability to act as competitive inhibitors for membrane proteoglycans, and modulate the inflammatory microenvironment of cancer cells. It is notable that SDCs and their soluble counterparts may affect either the behavior of cancer cells and/or their microenvironment during cancer progression. The importance of these molecules has been highlighted since HSPGs have been proposed as prognostic markers of solid tumors and hematopoietic malignancies. Going a step further down the line, the multi-actions of SDCs in many levels make them appealing as potential pharmacological targets, either by targeting directly the tumor or indirectly the adjacent stroma.

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Section: Tumor Microenvironment and Hspgsmentioning

confidence: 91%

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

et al. 2014

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“…Further studies demonstrated that syndecan-2 downregulation generates a decrease and reorganization of focal adhesions. This happened while actin was increasing its assembly, impairing a migratory behavior [137].…”

Section: Syndecan-2 In Angiogenesismentioning

confidence: 99%

Syndecans and Pancreatic Ductal Adenocarcinoma

et al. 2021

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Pancreatic Ductal Adenocarcinoma (PDAC) is a fatal disease with poor prognosis because patients rarely express symptoms in initial stages, which prevents early detection and diagnosis. Syndecans, a subfamily of proteoglycans, are involved in many physiological processes including cell proliferation, adhesion, and migration. Syndecans are physiologically found in many cell types and their interactions with other macromolecules enhance many pathways. In particular, extracellular matrix components, growth factors, and integrins collect the majority of syndecans associations acting as biochemical, physical, and mechanical transducers. Syndecans are transmembrane glycoproteins, but occasionally their extracellular domain can be released from the cell surface by the action of matrix metalloproteinases, converting them into soluble molecules that are capable of binding distant molecules such as extracellular matrix (ECM) components, growth factor receptors, and integrins from other cells. In this review, we explore the role of syndecans in tumorigenesis as well as their potential as therapeutic targets. Finally, this work reviews the contribution of syndecan-1 and syndecan-2 in PDAC progression and illustrates its potential to be targeted in future treatments for this devastating disease.

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“…Glycosaminoglycans have been implicated in atherosclerosis [145,146,147,148] and, indeed, three members of the glycosaminoglycan family, hyaluronan, heparan sulfate, and versican, have been shown to be TLR ligands. Hyaluronan (HA), upon injury, is degraded into various low-molecular-weight fragments that activate inflammatory processes in a variety of cell types, including endothelial cells, dendritic cells, and macrophages [149,150,151,152,153,154].…”

Section: Endogenous Ligandsmentioning

confidence: 99%

Toll-Like Receptors, Their Ligands, and Atherosclerosis

Hodgkinson

2011

The Scientific World JOURNAL

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Atherosclerosis is a disease characterized by inflammation in the arterial wall. Atherogenesis is dependent on the innate immune response involving activation of Toll-like receptors (TLRs) and the expression of inflammatory proteins. TLRs, which recognize various pathogen-associated molecular patterns, are expressed in various cell types within the atherosclerotic plaque. Microbial agents are associated with an increased risk of atherosclerosis and this is, in part, due to activation of TLRs. Recently considerable evidence has been provided suggesting that endogenous proteins promote atherosclerosis by binding to TLRs. In this review, we describe the role of TLRs in atherosclerosis with particular emphasis on those atherogenic endogenous proteins that have been implicated as TLR ligands.

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Is Syndecan-2 a Key Angiogenic Element?

Cited by 6 publications

References 38 publications

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

Syndecans and Pancreatic Ductal Adenocarcinoma

Toll-Like Receptors, Their Ligands, and Atherosclerosis

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