PMID- 28890654
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1177-2719 (Print)
IS  - 1177-2719 (Electronic)
IS  - 1177-2719 (Linking)
VI  - 12
DP  - 2017
TI  - Chondroitin Sulfate Inhibits Monocyte Chemoattractant Protein-1 Release From 
      3T3-L1 Adipocytes: A New Treatment Opportunity for Obesity-Related Inflammation?
PG  - 1177271917726964
LID - 10.1177/1177271917726964 [doi]
LID - 1177271917726964
AB  - 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 microg/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 microg/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 microg/mL and P < .001, 95% CI: -6.028 to -3.996 at 200 microg/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.
FAU - Stabler, Thomas V
AU  - Stabler TV
AD  - Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, 
      NC, USA.
FAU - Montell, Eulalia
AU  - Montell E
AD  - Pre-Clinical R&D Department, Bioiberica, S.A.U., Barcelona, Spain.
FAU - Verges, Josep
AU  - Verges J
AD  - Pre-Clinical R&D Department, Bioiberica, S.A.U., Barcelona, Spain.
FAU - Huebner, Janet L
AU  - Huebner JL
AD  - Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, 
      NC, USA.
FAU - Kraus, Virginia Byers
AU  - Kraus VB
AD  - Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, 
      NC, USA.
AD  - Division of Rheumatology and Immunology, Duke University School of Medicine, 
      Durham, NC, USA.
LA  - eng
PT  - Journal Article
DEP - 20170824
PL  - United States
TA  - Biomark Insights
JT  - Biomarker insights
JID - 101288638
PMC - PMC5574472
OTO - NOTNLM
OT  - Chondroitin sulfate
OT  - LPS
OT  - MCP-1
OT  - adipocytes
OT  - chemokines
COIS- Declaration of conflicting interests:The author(s) declared the following 
      potential conflicts of interest with respect to the research, authorship, and/or 
      publication of this article: E.M. and J.V. are employees of Bioiberica. 
      Bioiberica played no role in the decision to submit the manuscript for 
      publication. No nonfinancial conflicts exist for any of the authors.
EDAT- 2017/09/12 06:00
MHDA- 2017/09/12 06:01
PMCR- 2017/08/24
CRDT- 2017/09/12 06:00
PHST- 2017/06/06 00:00 [received]
PHST- 2017/07/27 00:00 [accepted]
PHST- 2017/09/12 06:00 [entrez]
PHST- 2017/09/12 06:00 [pubmed]
PHST- 2017/09/12 06:01 [medline]
PHST- 2017/08/24 00:00 [pmc-release]
AID - 10.1177_1177271917726964 [pii]
AID - 10.1177/1177271917726964 [doi]
PST - epublish
SO  - Biomark Insights. 2017 Aug 24;12:1177271917726964. doi: 10.1177/1177271917726964. 
      eCollection 2017.