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Isolation and characterization of human epicardial adipocytes: potential role in vascular inflammation

Adipose tissue is an important endocrine and secretory organ. There is growing evidence that adipocytes from different fat depots have distinct functional properties. Epicardial adipose tissue has been shown to produce inflammatory mediators, but the functional properties of isolated epicardial adip...

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Bibliographic Details
Published in:The FASEB journal 2006-03, Vol.20 (5), p.A1074-A1074
Main Authors: Stoll, Lynn L., Romig‐Martin, Sara A., Harrelson, Allan L., Snyder, Gary D., Adlakha, Satjit, Johnson, Bryon N., Fang, Xiang, Spector, Arthur A., Weintraub, Neal L.
Format: Article
Language:English
Online Access:Get full text
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Summary:Adipose tissue is an important endocrine and secretory organ. There is growing evidence that adipocytes from different fat depots have distinct functional properties. Epicardial adipose tissue has been shown to produce inflammatory mediators, but the functional properties of isolated epicardial adipocytes (EA) have not been studied. We characterized human EA isolated from freshly harvested hearts, along with subcutaneous and perirenal adipocytes from the same donors. Differentiation from preadipocytes was associated with greatly increased adipokine and proinflammatory cytokine expression; of note, the proinflammatory mediator CD14 was expressed at 50‐fold higher levels by EA compared to preadipocytes. EA have substantial cyclooxygenase and epoxide hydrolase activity. The major COX metabolite is PGE2, which plays an important role in angiogenesis and inflammation. LPS caused increased expression of adiponectin, VEGF, and CD14 in both epicardial adipose tissue explants and cultured EA. Conditioned medium from EA (but not control medium or medium from epicardial preadipocytes or subcutaneous adipocytes) strongly promoted growth and tubule formation by human coronary artery endothelial cells. These findings suggest that EA may play an important role in promoting coronary artery inflammation and growth of vasa vasorum and collateral coronary vessels in ischemia. (Supported by NIH HL70860 [NLW])
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.20.5.A1074-c