title: Coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue.
abstract: OBJECTIVE
  The purpose of this report was to assess the link between macrophage polarization in epicardial adipose tissue and atherosclerosis in patients with coronary artery disease (CAD).
  
  
  BACKGROUND
  Macrophage accumulation enhances chronic inflammation in adipose tissue, but macrophage phenotypic change in human epicardial adipose tissue and its role in atherogenesis are unknown.
  
  
  METHODS
  Samples were obtained from epicardial and subcutaneous adipose tissue during elective cardiac surgery (CAD, n = 38; non-CAD, n = 40). Infiltration of M1/M2 macrophages was investigated by immunohistochemical staining with antibodies against CD11c and CD206, respectively. Expression of pro- and anti-inflammatory adipocytokines in adipose tissue was evaluated by real-time quantitative polymerase chain reaction.
  
  
  RESULTS
  Infiltration of macrophages and expression of pro- and anti-inflammatory cytokines were enhanced in epicardial fat of patients with CAD compared with that in non-CAD patients (p < 0.05). The ratio of M1/M2 macrophages was positively correlated with the severity of CAD (r = 0.312, p = 0.039). Furthermore, the expression of pro-inflammatory cytokines was positively correlated, and the expression of anti-inflammatory cytokines was negatively correlated with the ratio of M1/M2 macrophages in epicardial adipose tissue of CAD patients. By contrast, there was no significant difference in macrophage infiltration and cytokine expression in subcutaneous adipose tissue between the CAD and non-CAD groups.
  
  
  CONCLUSIONS
  The ratio of M1/M2 macrophages in epicardial adipose tissue of CAD patients is changed compared with that in non-CAD patients. Human coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue.
authors: Department of Cardiovascular Medicine, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.
authors: Yoichiro
authors: Y
authors: Hirata
authors: Minoru
authors: M
authors: Tabata
authors: Hirotsugu
authors: H
authors: Kurobe
authors: Tatsuo
authors: T
authors: Motoki
authors: Masashi
authors: M
authors: Akaike
authors: Chika
authors: C
authors: Nishio
authors: Mayuko
authors: M
authors: Higashida
authors: Hiroaki
authors: H
authors: Mikasa
authors: Yutaka
authors: Y
authors: Nakaya
authors: Shuichiro
authors: S
authors: Takanashi
authors: Takashi
authors: T
authors: Igarashi
authors: Tetsuya
authors: T
authors: Kitagawa
authors: Masataka
authors: M
authors: Sata
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D039521:CD11c Antigen / Q000032:analysis; D018932:Chemokine CCL2 / Q000378:metabolism; D003324:Coronary Artery Disease / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D037181:Lectins, C-Type / Q000032:analysis; D008264:Macrophages / Q000378:metabolism / Q000473:pathology*; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000032:analysis; D010496:Pericardium / Q000473:pathology*; D011956:Receptors, Cell Surface / Q000032:analysis; D050151:Subcutaneous Fat / Q000473:pathology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D039521:CD11c Antigen; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D011956:Receptors, Cell Surface; C067980:CD68 antigen, human; D000097382:CD68 Molecule