• ISSN 16748301
  • CN 32-1810/R
Volume 28 Issue 3
May  2014
Article Contents

Citation:

Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage

  • Received Date: 2013-07-10
  • Macrophage death in advanced atherosclerosis promotes plaque necrosis and destabilization. Autophagy func?tions in bulk degradation of cellular components, has been recognized recently as an important mechanism for cell survive under endoplasmic reticulum (ER) stress. We previously found that engagement of the class A scavenger receptor (SR-A) triggered JNK-dependent apoptosis in ER-stressed macrophages. However, the pro-apoptosis mechanisms mediated by SR-A are not fully understood. We therefore sought to see if SR-A mediated apoptosis was associated with the autophagy in macrophages. In this study, we showed that fucoidan inhibited microtubule-associated protein light chain 3-phospholipid conjugates (LC3-II) formation as well as the number of autophago?somes under ER stress. The inhibition of LC3-II formation was paralleled by activation of mTOR pathways, and inhibition of mTOR allowed LC3-II induction in macrophages treated with thapsigargin plus fucoidan. Further?more, apoptosis induced by fucoidan was prevented under ER stress by the inhibitor of mTOR treatment. We propose that fucoidan, a SR-A agonist, may contribute to macrophages apoptosis during ER stress by inhibition of autophagy.
  • 加载中
  • 加载中

Article Metrics

Article views(1612) PDF downloads(5713) Cited by()

Related
Proportional views
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage

  • 1. Atherosclerosis Research Centre, Laboratory of Molecular Intervention with Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China
  • 2.  State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China
  • 3. State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China

Abstract: Macrophage death in advanced atherosclerosis promotes plaque necrosis and destabilization. Autophagy func?tions in bulk degradation of cellular components, has been recognized recently as an important mechanism for cell survive under endoplasmic reticulum (ER) stress. We previously found that engagement of the class A scavenger receptor (SR-A) triggered JNK-dependent apoptosis in ER-stressed macrophages. However, the pro-apoptosis mechanisms mediated by SR-A are not fully understood. We therefore sought to see if SR-A mediated apoptosis was associated with the autophagy in macrophages. In this study, we showed that fucoidan inhibited microtubule-associated protein light chain 3-phospholipid conjugates (LC3-II) formation as well as the number of autophago?somes under ER stress. The inhibition of LC3-II formation was paralleled by activation of mTOR pathways, and inhibition of mTOR allowed LC3-II induction in macrophages treated with thapsigargin plus fucoidan. Further?more, apoptosis induced by fucoidan was prevented under ER stress by the inhibitor of mTOR treatment. We propose that fucoidan, a SR-A agonist, may contribute to macrophages apoptosis during ER stress by inhibition of autophagy.

    HTML

Catalog

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return