scholarly journals Aflatoxin B1 affects apoptosis and expression of death receptor and endoplasmic reticulum molecules in chicken spleen

Oncotarget ◽  
2017 ◽  
Vol 8 (59) ◽  
pp. 99531-99540 ◽  
Author(s):  
Panpan Zhu ◽  
Zhicai Zuo ◽  
Zhixiang Zheng ◽  
Fengyuan Wang ◽  
Xi Peng ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Aflatoxin B1 ◽  
Death Receptor ◽  
Chicken Spleen

scholarly journals Endoplasmic reticulum calcium pool depletion-induced apoptosis is coupled with activation of the death receptor 5 pathway

Oncogene ◽  
2002 ◽  
Vol 21 (17) ◽  
pp. 2623-2633 ◽  
Author(s):  
Qin He ◽  
Dong Ik Lee ◽  
Rong Rong ◽  
Myounghee Yu ◽  
Xiuquan Luo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Endoplasmic Reticulum Calcium ◽  
Induced Apoptosis ◽  
Calcium Pool

scholarly journals Role of Endoplasmic Reticulum Stress in α-TEA Mediated TRAIL/DR5 Death Receptor Dependent Apoptosis

PLoS ONE ◽  
2010 ◽  
Vol 5 (7) ◽  
pp. e11865 ◽  
Author(s):  
Richa Tiwary ◽  
Weiping Yu ◽  
Jing Li ◽  
Sook-Kyung Park ◽  
Bob G. Sanders ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Death Receptor

scholarly journals Autocrine Tumor Necrosis Factor Alpha Links Endoplasmic Reticulum Stress to the Membrane Death Receptor Pathway through IRE1α-Mediated NF-κB Activation and Down-Regulation of TRAF2 Expression

2006 ◽  
Vol 26 (8) ◽  
pp. 3071-3084 ◽  
Author(s):  
Ping Hu ◽  
Zhang Han ◽  
Anthony D. Couvillon ◽  
Randal J. Kaufman ◽  
John H. Exton
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Er Stress ◽  
Tumor Necrosis ◽  
Death Receptor ◽  
Down Regulation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT NF-κB is critical for determining cellular sensitivity to apoptotic stimuli by regulating both mitochondrial and death receptor apoptotic pathways. The endoplasmic reticulum (ER) emerges as a new apoptotic signaling initiator. However, the mechanism by which ER stress activates NF-κB and its role in regulation of ER stress-induced cell death are largely unclear. Here, we report that, in response to ER stress, IKK forms a complex with IRE1α through the adapter protein TRAF2. ER stress-induced NF-κB activation is impaired in IRE1α knockdown cells and IRE1α−/− MEFs. We found, however, that inhibiting NF-κB significantly decreased ER stress-induced cell death in a caspase-8-dependent manner. Gene expression analysis revealed that ER stress-induced expression of tumor necrosis factor alpha (TNF-α) was IRE1α and NF-κB dependent. Blocking TNF receptor 1 signaling significantly inhibited ER stress-induced cell death. Further studies suggest that ER stress induces down-regulation of TRAF2 expression, which impairs TNF-α-induced activation of NF-κB and c-Jun N-terminal kinase and turns TNF-α from a weak to a powerful apoptosis inducer. Thus, ER stress induces two signals, namely TNF-α induction and TRAF2 down-regulation. They work in concert to amplify ER-initiated apoptotic signaling through the membrane death receptor.

scholarly journals Colistin-Induced Nephrotoxicity in Mice Involves the Mitochondrial, Death Receptor, and Endoplasmic Reticulum Pathways

2014 ◽  
Vol 58 (7) ◽  
pp. 4075-4085 ◽  
Author(s):  
Chongshan Dai ◽  
Jichang Li ◽  
Shusheng Tang ◽  
Jian Li ◽  
Xilong Xiao
Keyword(s):  
Endoplasmic Reticulum ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Protective Role ◽  
Limiting Factor ◽  
Death Domain ◽  
Tubular Necrosis ◽  
Apoptosis Pathways ◽  
Group A ◽  
Induced Apoptosis

ABSTRACTNephrotoxicity is the dose-limiting factor for colistin, but the exact mechanism is unknown. This study aimed to investigate the roles of the mitochondrial, death receptor, and endoplasmic reticulum pathways in colistin-induced nephrotoxicity. Mice were intravenously administered 7.5 or 15 mg of colistin/kg of body weight/day (via a 3-min infusion and divided into two doses) for 7 days. Renal function, oxidative stress, and apoptosis were measured. Representative biomarkers involved in the mitochondrial, death receptor, and endoplasmic reticulum pathways were investigated, and the key markers involved in apoptosis and autophagy were examined. After 7-day colistin treatment, significant increase was observed with blood urea nitrogen, serum creatinine, and malondialdehyde, while activities of superoxide dismutase (SOD) and catalase decreased in the kidneys. Acute tubular necrosis and mitochondrial dysfunction were detected, and colistin-induced apoptosis was characterized by DNA fragmentation, cleavage of poly(ADP-ribose) polymerase (PARP-1), increase of 8-hydroxydeoxyguanosine (8-OHdG), and activation of caspases (caspase-8, -9, and -3). It was evident that colistin-induced apoptosis involved the mitochondrial pathway (downregulation of Bcl-2 and upregulation of cytochrome C [cytC] and Bax), death receptor pathway (upregulation of Fas, FasL, and Fas-associated death domain [FADD]), and endoplasmic reticulum pathway (upregulation of Grp78/Bip, ATF6, GADD153/CHOP, and caspase-12). In the 15-mg/kg/day colistin group, expression of the cyclin-dependent kinase 2 (CDK2) and phosphorylated JNK (p-JNK) significantly increased (P< 0.05), while in the 7.5-mg/kg/day colistin group, a large number of autophagolysosomes and classic autophagy were observed. Western blot results of Beclin-1 and LC3B indicated that autophagy may play a protective role in colistin-induced nephrotoxicity. In conclusion, this is the first study to demonstrate that all three major apoptosis pathways and autophagy are involved in colistin-induced nephrotoxicity.

scholarly journals A study on the expression of apoptotic molecules related to death receptor and endoplasmic reticulum pathways in the jejunum of AFB1-intoxicated chickens

Oncotarget ◽  
2017 ◽  
Vol 8 (52) ◽  
pp. 89655-89664 ◽  
Author(s):  
Zhixiang Zheng ◽  
Zhicai Zuo ◽  
Panpan Zhu ◽  
Fengyuan Wang ◽  
Heng Yin ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Death Receptor
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