Three-Dimensional Migration of Human Adult Dermal Fibroblasts from Collagen Lattices into Fibrin/Fibronectin Gels Requires Syndecan-4 Proteoglycan

Lin, Fubao; Ren, Xiang‐Dong; Greiling, Doris; Clark, Richard A.F.

doi:10.1111/j.0022-202x.2005.23740.x

Cited by 48 publications

(35 citation statements)

References 33 publications

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“…Different mechanisms that underlie the migration of cells across fibronectin and the invasion of cells through Matrigel, a reconstituted basement membrane, might account for this differential activity in movement. On one hand, heparan sulfate chains carried by proteoglycans, such as syndecan-4, are highly involved in cell adherence to fibronectin and in cell mobility across fibronectin (45,46). Moreover, we previously showed that RANTES/CCL5 associates with syndecan-4 and syndecan-1 in a glycosaminoglycandependent manner on HeLa and macrophage cell surfaces (8,9).…”

Section: Discussionmentioning

confidence: 99%

Glycosaminoglycans and their synthetic mimetics inhibit RANTES-induced migration and invasion of human hepatoma cells

Sutton

Friand

Papy-García

et al. 2007

Molecular Cancer Therapeutics

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The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein -coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans. This study was undertaken to investigate whether this chemokine is involved in hepatoma cell migration or invasion and to modulate these effects in vitro by the use of glycosaminoglycan mimetics. We show that the human hepatoma Huh7 and Hep3B cells express RANTES/CCL5 G protein -coupled receptor CCR1 but not CCR3 nor CCR5. RANTES/CCL5 binding to these cells depends on CCR1 and glycosaminoglycans. Moreover, RANTES/CCL5 strongly stimulates the migration and the invasion of Huh7 cells and to a lesser extent that of Hep3B cells. RANTES/CCL5 also stimulates the tyrosine phosphorylation of focal adhesion kinase and activates matrix metalloproteinase-9 in Huh7 hepatoma cells, resulting in increased invasion of these cells. The fact that RANTES/CCL5-induced migration and invasion of Huh7 cells are both strongly inhibited by anti-CCR1 antibodies and heparin, as well as by B-D-xyloside treatment of the cells, suggests that CCR1 and glycosaminoglycans are involved in these events. We then show by surface plasmon resonance that synthetic glycosaminoglycan mimetics, OTR4120 or OTR4131, directly bind to RANTES/CCL5. The preincubation of the chemokine with each of these mimetics strongly inhibited RANTES-induced migration and invasion of Huh7 cells. Therefore, targeting the RANTES-glycosaminoglycan interaction could be a new therapeutic approach for human hepatocellular carcinoma. [Mol Cancer Ther 2007;6(11):2948 -58]

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Section: Discussionmentioning

confidence: 99%

Glycosaminoglycans and their synthetic mimetics inhibit RANTES-induced migration and invasion of human hepatoma cells

Sutton

Friand

Papy-García

et al. 2007

Molecular Cancer Therapeutics

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“…Syndecan-4 has been shown to affect wound healing, resulting in delayed closure of skin incisions in its absence (20). Syndecan-4 is required for dermal fibroblast invasive migration into fibrin clot (34). We identified Sdc4 as a gene induced in response to lung injury and sought to determine its role in lung inflammation and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of pulmonary fibrosis in mice by CXCL10 requires glycosaminoglycan binding and syndecan-4

Jiang¹,

Liang²,

Campanella³

et al. 2010

J. Clin. Invest.

146

130

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Pulmonary fibrosis is a progressive, dysregulated response to injury culminating in compromised lung function due to excess extracellular matrix production. The heparan sulfate proteoglycan syndecan-4 is important in mediating fibroblast-matrix interactions, but its role in pulmonary fibrosis has not been explored. To investigate this issue, we used intratracheal instillation of bleomycin as a model of acute lung injury and fibrosis. We found that bleomycin treatment increased syndecan-4 expression. Moreover, we observed a marked decrease in neutrophil recruitment and an increase in both myofibroblast recruitment and interstitial fibrosis in bleomycin-treated syndecan-4-null (Sdc4 -/-) mice. Subsequently, we identified a direct interaction between CXCL10, an antifibrotic chemokine, and syndecan-4 that inhibited primary lung fibroblast migration during fibrosis; mutation of the heparin-binding domain, but not the CXCR3 domain, of CXCL10 diminished this effect. Similarly, migration of fibroblasts from patients with pulmonary fibrosis was inhibited in the presence of CXCL10 protein defective in CXCR3 binding. Furthermore, administration of recombinant CXCL10 protein inhibited fibrosis in WT mice, but not in Sdc4 -/-mice. Collectively, these data suggest that the direct interaction of syndecan-4 and CXCL10 in the lung interstitial compartment serves to inhibit fibroblast recruitment and subsequent fibrosis. Thus, administration of CXCL10 protein defective in CXCR3 binding may represent a novel therapy for pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

“…For example, syndecan 4 is essential for the invasion of fibroblasts into fibrin clots (42). Further, platelet-derived growth factor, the stimulus for migration, induces syndecan 4 core protein expression (42). Syndecan 1 is required for keratinocyte invasion across a laminin matrix and for the Rac-mediated formation of invadopodia (43).…”

Section: Discussionmentioning

confidence: 99%

Heparan Sulfate Proteoglycan Modulation of Wnt5A Signal Transduction in Metastatic Melanoma Cells

O’Connell

Fiori

Kershner

et al. 2009

Journal of Biological Chemistry

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Heparan sulfate proteoglycans (HSPGs) are important modulators for optimizing signal transduction of many pathways, including the Wnt pathways. We demonstrate that HSPG glycosaminoglycan levels increased with increasing metastatic potential of melanoma cells. Previous studies have demonstrated that Wnt5A increases the invasiveness of melanoma cells. We further demonstrate that HSPGs potentiate Wnt5A signaling, since enzymatic removal of the HSPG backbone resulted in a decrease in cellular Wnt5A levels, an increase in secreted Wnt5A in cell media, a decrease in downstream signaling, and ultimately, a decrease in invasiveness. Specifically, syndecan 1 and syndecan 4 expression correlated to Wnt5A expression and melanoma malignancy. Knockdown of syndecan 1 or 4 caused decreases in cell invasion, which could be restored by treating the cells with recombinant Wnt5A. These data indicate that syndecan 1 and 4 correlate to increased metastatic potential in melanoma patients and are an important component of the Wnt5A autocrine signaling loop, the activation of which leads to increased metastasis of melanoma.

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Three-Dimensional Migration of Human Adult Dermal Fibroblasts from Collagen Lattices into Fibrin/Fibronectin Gels Requires Syndecan-4 Proteoglycan

Cited by 48 publications

References 33 publications

Glycosaminoglycans and their synthetic mimetics inhibit RANTES-induced migration and invasion of human hepatoma cells

Glycosaminoglycans and their synthetic mimetics inhibit RANTES-induced migration and invasion of human hepatoma cells

Inhibition of pulmonary fibrosis in mice by CXCL10 requires glycosaminoglycan binding and syndecan-4

Heparan Sulfate Proteoglycan Modulation of Wnt5A Signal Transduction in Metastatic Melanoma Cells

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