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Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism.
Wang, Jing; Chen, Dong; Cheng, Xun-Min; Zhang, Qi-Gao; Peng, Yong-Ping; Wang, Li-Jun; He, Song-Qing; Gong, Jian-Bin.
Afiliación
  • Wang J; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Chen D; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Cheng XM; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Zhang QG; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Peng YP; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Wang LJ; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • He SQ; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
  • Gong JB; Department of Cardiology, Jinling Hospital, School of Clinical Medicine, Nanjing University No. 305 East Zhongshan Rd., Nanjing 210002, China.
Am J Transl Res ; 7(10): 1712-23, 2015.
Article en En | MEDLINE | ID: mdl-26692919
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). CONCLUSION: 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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Am J Transl Res Año: 2015 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Am J Transl Res Año: 2015 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos