The Role of Endoplasmic Reticulum Stress in Silica-Induced Apoptosis in Alveolar Macrophages

CHEST Journal ◽  
2016 ◽  
Vol 149 (4) ◽  
pp. A415
Author(s):  
Yongbin Hu ◽  
Xia Wu ◽  
Pinhua Pan
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Alveolar Macrophages ◽  
Induced Apoptosis

scholarly journals The Chondroprotective Role of TMF in PGE2-Induced Apoptosis Associating with Endoplasmic Reticulum Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jianqiong Yang ◽  
Haiqing Liu ◽  
Linfu Li ◽  
Hai Liu ◽  
Weimei Shi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Inflammatory Cytokine ◽  
Critical Role ◽  
Osteoarthritic Chondrocytes ◽  
Induced Apoptosis

Endoplasmic reticulum stress (ERS) has been demonstrated to exhibit a critical role in osteoarthritic chondrocytes. Whether 5,7,3′,4′-tetramethoxyflavone (TMF) plays the chondroprotective role in inhibition of PGE2-induced chondrocytes apoptosis associating with ERS has not been reported. To investigate this, the activation of PERK, ATF6, and IRE1 signaling pathways in ERS in chondrocytes pretreated with PGE2was studied. By treatment with PGE2, the chondrocytes apoptosis was significantly increased, the proapoptotic CHOP and JNK were upregulated, the prosurvival GRP78 and XBP1 were downregulated, and GSK-3βwas also upregulated. However, TMF exhibited the effectively protective functions via counteracting these detrimental effects of PGE2. Finally, the inflammatory cytokine PGE2can activate ERS signaling and promote chondrocytes apoptosis, which might be associated with upregulation of GSK-3β. TMF exhibits a chondroprotective role in inhibiting PGE2-induced ERS and GSK-3β.

The role of GRP78, p-ERK and Bcl-2 proteins in endoplasmic reticulum stress-induced apoptosis and anti-apoptosis in melanoma

Pathology ◽  
2009 ◽  
Vol 41 ◽  
pp. 67-68
Author(s):  
Liqing Zhuang ◽  
Richard A. Scolyer ◽  
Stanley W. McCarthy ◽  
Xu Dong Zhang ◽  
Peter Hersey
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Induced Apoptosis
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