Low molecular mass dermatan sulfate modulates endothelial cells proliferation and migration

Rasente, Rita Yanina; Egitto, Paula; Calabrese, Graciela Cristina

doi:10.1016/j.carres.2012.03.036

Cited by 11 publications

(13 citation statements)

References 26 publications

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“…D and NO stimulation. MMP-2 involvement in PAE cells migration well correlated with previous studies reporting a constitutive MMP-2 expression in endothelium [27,29], and its upregulation during endothelial cells migration and tube formation in a 3D matrix [30]. …”

Section: Discussionsupporting

confidence: 86%

“…Extracellular matrix (ECM) degradation allows vascular endothelial cells to migrate through their basal membrane and mainly involves matrix metalloproteinases (MMPs) activity. MMPs constitute a tightly regulated family of endogenous zinc dependent endopeptidases, divided into different subfamilies according to their substrate specificity, degrading most of the components of ECM and basal membrane [27,28]. In particular, the main components of vascular basal lamina (collagen IV, laminin and fibronectin), are degraded mainly by MMP-2 and MMP-9, also known as gelatinases [29].…”

Section: Discussionmentioning

confidence: 99%

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1a,25-Dihydroxycholecalciferol (Vitamin D3) Induces NO-Dependent Endothelial Cell Proliferation and Migration in a Three-Dimensional Matrix

Molinari

Rizzi

Squarzanti

et al. 2013

Cell Physiol Biochem

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Background/Aims: The 1α,25-dihydroxycholecalciferol (Vit. D) induces eNOS dependent nitric oxide (NO) production in human umbilical vein endothelial cells (HUVEC). To our knowledge, there are no reports directly relating Vit. D induced NO production to proliferation and/or migration in endothelial cells (EC). The aim of this study was to evaluate whether Vit. D addition to porcine EC could affect their proliferation and/or migration in a three-dimensional matrix via NO production. Materials and Methods: Porcine aortic endothelial cells (PAE) were used to evaluate Vit. D effects on cell proliferation and migration in a three-dimensional matrix. Results: Vit. D induced NO production in PAE cells. Moreover, it induced a significant increase in cellular proliferation and migration in a three-dimensional matrix. These effects were NO dependent, as inhibiting eNOS activity by L-NAME PAE migration was abrogated. This effect was strictly related to MMP-2 expression and apparently dependent on Vit. D and NO production. Conclusions: Vit. D can promote both endothelial cells proliferation and migration in a three-dimensional matrix via NO-dependent mechanisms. These findings cast new light on the role of Vit. D in the angiogenic process, suggesting new applications for Vit. D in such fields as tissue repair and wound healing.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

1a,25-Dihydroxycholecalciferol (Vitamin D3) Induces NO-Dependent Endothelial Cell Proliferation and Migration in a Three-Dimensional Matrix

Molinari

Rizzi

Squarzanti

et al. 2013

Cell Physiol Biochem

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“…In most of the reports CS/DS-PGs and CS/DS free chains were exogenously added [39], [40] or removed by enzymatic digestion [20], showing contradictory results. For instance, decorin was shown to slow the migration rate of osteosarcoma cells by a mechanism depending on its CS/DS chain [28], while CS/DS-PGs biglycan and decorin, independently of their CS/DS, increased mobility of lung fibroblasts [39].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, decorin was shown to slow the migration rate of osteosarcoma cells by a mechanism depending on its CS/DS chain [28], while CS/DS-PGs biglycan and decorin, independently of their CS/DS, increased mobility of lung fibroblasts [39]. Moreover, addition of low molecular weight CS/DS stimulated migration of endothelial cells [40]. We could establish that CS/DS-PGs, either supplied in conditioned media or in pre-deposited ECM, failed to alter the motility of WT and DS-epi1−/− cells, which indicates that the mechanism behind the change of migration and adhesion is related to cell surface CS/DS-PGs.…”

Section: Discussionmentioning

confidence: 99%

Iduronic Acid in Chondroitin/Dermatan Sulfate Affects Directional Migration of Aortic Smooth Muscle Cells

et al. 2013

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Aortic smooth muscle cells produce chondroitin/dermatan sulfate (CS/DS) proteoglycans that regulate extracellular matrix organization and cell behavior in normal and pathological conditions. A unique feature of CS/DS proteoglycans is the presence of iduronic acid (IdoA), catalyzed by two DS epimerases. Functional ablation of DS-epi1, the main epimerase in these cells, resulted in a major reduction of IdoA both on cell surface and in secreted CS/DS proteoglycans. Downregulation of IdoA led to delayed ability to re-populate wounded areas due to loss of directional persistence of migration. DS-epi1−/− aortic smooth muscle cells, however, had not lost the general property of migration showing even increased speed of movement compared to wild type cells. Where the cell membrane adheres to the substratum, stress fibers were denser whereas focal adhesion sites were fewer. Total cellular expression of focal adhesion kinase (FAK) and phospho-FAK (pFAK) was decreased in mutant cells compared to control cells. As many pathological conditions are dependent on migration, modulation of IdoA content may point to therapeutic strategies for diseases such as cancer and atherosclerosis.

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“…Dermatan sulphate could play protective roles in the arterial wall. It is known that DS chains greatly increase the rate of thrombin inhibition by heparin cofactor II, providing the tissue with anti-atherogenic properties, as thrombin is thought to contribute to atherogenesis, influencing coagulation, chemoattraction and proliferation (Tollefsen 2010;Rasente et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Atheroprotective remodelling of vascular dermatan sulphate proteoglycans in response to hypercholesterolaemia in a rat model

Oberkersch

Maccari

Bravo³

et al. 2014

Int J Experimental Path

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Proteoglycan accumulation within the arterial intima has been implicated in atherosclerosis progression in humans. Nevertheless, hypercholesterolaemia is unable to induce intimal thickening and atheroma plaque development in rats. The study was performed to analyse proteoglycans modifications in rats fed with a high-cholesterol diet to understand whether vascular wall remodelling protects against lesions. Sections obtained from rat aortas showed normal features, in intimal-to-media ratio and lipid accumulation. However, focal endothelial hyperplasia and neo-intima rearrangement were observed in high-cholesterol animals. Besides, hypercholesterolaemia induced an inflammatory microenviroment. We determined the expression of different proteoglycans from aortic cells by Western blot and observed a diminished production of decorin and biglycan in high-cholesterol animals compared with control (P < 0.01 and P < 0.05, respectively). Versican was increased in high-cholesterol animals (P < 0.05), whereas perlecan production showed no differences. No modification of the total content of glycosaminoglycans (GAGs) was found between the two experimental groups. In contrast, the chondroitin sulphate/dermatan sulphate ratio was increased in the high-cholesterol group as compared to the control (0.56 and 0.34, respectively). Structural alterations in the disaccharide composition of galactosaminoglycans were also detected by HPLC, as the ratio of 6-sulphate to 4-sulphate disaccharides was increased in high-cholesterol animals (P < 0.05). Our results suggest that attenuation of decorin and biglycan expression might be an effective strategy to inhibit the first step in atherogenesis, although specific GAG structural modification associated with the development of vascular disease took place. Results emphasize the potential application of therapies based on vascular matrix remodelling to treat atherosclerosis.

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Low molecular mass dermatan sulfate modulates endothelial cells proliferation and migration

Cited by 11 publications

References 26 publications

1a,25-Dihydroxycholecalciferol (Vitamin D3) Induces NO-Dependent Endothelial Cell Proliferation and Migration in a Three-Dimensional Matrix

1a,25-Dihydroxycholecalciferol (Vitamin D3) Induces NO-Dependent Endothelial Cell Proliferation and Migration in a Three-Dimensional Matrix

Iduronic Acid in Chondroitin/Dermatan Sulfate Affects Directional Migration of Aortic Smooth Muscle Cells

Atheroprotective remodelling of vascular dermatan sulphate proteoglycans in response to hypercholesterolaemia in a rat model

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