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C-reactive protein inhibits high-molecular-weight adiponectin expression in 3T3-L1 adipocytes via PI3K/Akt pathway
被引:5
作者:
Liu, Yuanxin
[1
]
Liu, Cuiping
[2
]
Jiang, Chao
[2
]
Wang, Su
[1
]
Yang, Qichao
[1
]
Jiang, Dan
[1
]
Yuan, Guoyue
[1
]
机构:
[1] Jiangsu Univ, Affiliated Hosp, Dept Endocrinol, 438 Jiefang Rd, Zhenjiang 212001, Peoples R China
[2] Najing Med Univ, Affiliated Hosp 1, Publ Lab Platform, Nanjing 210029, Jiangsu, Peoples R China
关键词:
INSULIN-RESISTANCE;
ADIPOSE-TISSUE;
SIGNALING PATHWAY;
INFLAMMATION;
MULTIMERIZATION;
ASSOCIATION;
SECRETION;
OBESITY;
ACTIVATION;
GLUCOSE;
D O I:
10.1016/j.bbrc.2016.01.143
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Adiponectin, an adipose-specific protein hormone, is secreted from white adipose tissue and involved in glucose and lipid metabolism. It is assembled into low-molecular-weight trimer (LMW), middle molecular-weight hexameric (MMW) and high-molecular-weight (HMW), among which HMW exhibits higher activity. In this study, we proved that C-reactive protein (CRP), an inflammatory marker, inhibited adiponectin expression, especially HMW in time-and dose-dependent manners. Furthermore, CRP decreased the HMW/total adiponectin ration and reduced adiponectin assembly by increasing ERp44, and decreasing Ero1-alpha and DsbA-L. CRP activated pAkt, the downstream of PI3K. Inhibition of PI3K or pAkt abolished the effect of CRP. Our study suggested that CRP decreased adiponectin expression and multimerization, while CRP-induced decline in adiponectin might be mediated through the PI3K/Akt pathway. (C) 2016 Elsevier Inc. All rights reserved.
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页码:19 / 25
页数:7
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