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.
引用
收藏
页码:19 / 25
页数:7
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