Chondroitin Sulfate Inhibits Monocyte Chemoattractant Protein-1 Release From 3T3-L1 Adipocytes: A New Treatment Opportunity for Obesity-Related Inflammation?
| dc.contributor.author | Stabler, Thomas V | |
| dc.contributor.author | Montell, Eulàlia | |
| dc.contributor.author | Vergés, Josep | |
| dc.contributor.author | Huebner, Janet L | |
| dc.contributor.author | Kraus, Virginia Byers | |
| dc.date.accessioned | 2019-02-02T15:31:37Z | |
| dc.date.available | 2019-02-02T15:31:37Z | |
| dc.date.issued | 2017-01 | |
| dc.date.updated | 2019-02-02T15:31:36Z | |
| dc.description.abstract | Monocyte chemoattractant protein-1 (MCP-1) overproduction from inflamed adipose tissue is a major contributor to obesity-related metabolic syndromes. 3T3-L1 embryonic fibroblasts were cultured and differentiated into adipocytes using an established protocol. Adipocytes were treated with lipopolysaccharide (LPS) to induce inflammation and thus MCP-1 release. At the same time, varying concentrations of chondroitin sulfate (CS) were added in a physiologically relevant range (10-200 µg/mL) to determine its impact on MCP-1 release. Chondroitin sulfate, a natural glycosaminoglycan of connective tissue including the cartilage extracellular matrix, was chosen on the basis of our previous studies demonstrating its anti-inflammatory effect on macrophages. Because the main action of MCP-1 is to induce monocyte migration, cultured THP-1 monocytes were used to test whether CS at the highest physiologically relevant concentration could inhibit cell migration induced by human recombinant MCP-1. Chondroitin sulfate (100-200 µg/mL) inhibited MCP-1 release from inflamed adipocytes in a dose-dependent manner (P < .01, 95% confidence interval [CI]: -5.89 to -3.858 at 100 µg/mL and P < .001, 95% CI: -6.028 to -3.996 at 200 µg/mL) but had no effect on MCP-1-driven chemotaxis of THP-1 monocytes. In summary, CS could be expected to reduce macrophage infiltration into adipose tissue by reduction in adipocyte expression and release of MCP-1 and as such might reduce adipose tissue inflammation in response to pro-inflammatory stimuli such as LPS, now increasingly recognized to be relevant in vivo. | |
| dc.identifier | 10.1177_1177271917726964 | |
| dc.identifier.issn | 1177-2719 | |
| dc.identifier.issn | 1177-2719 | |
| dc.identifier.uri | ||
| dc.language | eng | |
| dc.publisher | SAGE Publications | |
| dc.relation.ispartof | Biomarker insights | |
| dc.relation.isversionof | 10.1177/1177271917726964 | |
| dc.subject | Chondroitin sulfate | |
| dc.subject | LPS | |
| dc.subject | MCP-1 | |
| dc.subject | adipocytes | |
| dc.subject | chemokines | |
| dc.title | Chondroitin Sulfate Inhibits Monocyte Chemoattractant Protein-1 Release From 3T3-L1 Adipocytes: A New Treatment Opportunity for Obesity-Related Inflammation? | |
| dc.type | Journal article | |
| duke.contributor.orcid | Kraus, Virginia Byers|0000-0001-8173-8258 | |
| pubs.begin-page | 1177271917726964 | |
| pubs.organisational-group | School of Medicine | |
| pubs.organisational-group | Duke | |
| pubs.organisational-group | Duke Molecular Physiology Institute | |
| pubs.organisational-group | Institutes and Centers | |
| pubs.organisational-group | Orthopaedics | |
| pubs.organisational-group | Clinical Science Departments | |
| pubs.organisational-group | Pathology | |
| pubs.organisational-group | Medicine, Rheumatology and Immunology | |
| pubs.organisational-group | Medicine | |
| pubs.publication-status | Published | |
| pubs.volume | 12 |
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