C-reactive protein inhibits high-molecular-weight adiponectin expression in 3T3-L1 adipocytes via PI3K/Akt pathway

C-reactive protein inhibits high-molecular-weight adiponectin expression in 3T3-L1 adipocytes via PI3K/Akt pathway
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C反应蛋白通过PI3K/Akt途径抑制3T3-L1脂肪细胞中高分子量脂联素的表达

DOI:
10.1016/j.bbrc.2016.01.143
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发表时间:
2016-03-25
影响因子:
3.1
通讯作者:
Yuan, Guoyue
Yuan, Guoyue
中科院分区:
生物学4区
文献类型:
--
作者:
Liu, Yuanxin;Liu, Cuiping;Yuan, Guoyue

文献摘要

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脂联素是一种脂肪特异性蛋白激素,由白色脂肪组织分泌,参与糖脂代谢。它被组装成低分子量三聚体(LMW)、中分子量六聚体(MMW)和高分子量三聚体(HMW),其中HMW具有较高的活性。在这项研究中,我们证明了炎症标志物c反应蛋白(CRP)以时间和剂量依赖的方式抑制脂联素的表达,尤其是HMW。此外,CRP通过增加ERp44、降低ero1 - α和DsbA-L来降低HMW/总脂联素比率和减少脂联素组装。CRP激活pAkt, PI3K的下游。抑制PI3K或pAkt可消除CRP的作用。我们的研究表明,CRP降低了脂联素的表达和聚合,而CRP诱导的脂联素的下降可能通过PI3K/Akt途径介导。(C) 2016 Elsevier Inc.版权所有。
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.