title: Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism.
abstract: OBJECTIVE
  To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis.
  
  
  METHODS
  A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
  
  
  RESULTS
  At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05).
  
  
  CONCLUSIONS
  During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Xun-Min
authors.initials: XM
authors.lastname: Cheng
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Qi-Gao
authors.initials: QG
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Yong-Ping
authors.initials: YP
authors.lastname: Peng
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Song-Qing
authors.initials: SQ
authors.lastname: He
authors.affiliation: Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
authors.forename: Jian-Bin
authors.initials: JB
authors.lastname: Gong
keywords: Epicardiac adipose tissue; IL-6; STAT; atherosclerosis; cellular phenotype