• ISSN 1674-8301
  • CN 32-1810/R
Volume 28 Issue 3
May  2014
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Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen. Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage[J]. The Journal of Biomedical Research, 2014, 28(3): 213-221. doi: 10.7555/JBR.28.20130105
Citation: Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen. Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage[J]. The Journal of Biomedical Research, 2014, 28(3): 213-221. doi: 10.7555/JBR.28.20130105

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

doi: 10.7555/JBR.28.20130105
  • Received Date: 2013-07-10
  • Publish Date: 2014-05-28
  • 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.
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    沈阳化工大学材料科学与工程学院 沈阳 110142

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

doi: 10.7555/JBR.28.20130105

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.

Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen. Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage[J]. The Journal of Biomedical Research, 2014, 28(3): 213-221. doi: 10.7555/JBR.28.20130105
Citation: Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen. Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage[J]. The Journal of Biomedical Research, 2014, 28(3): 213-221. doi: 10.7555/JBR.28.20130105

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