scholarly journals Ginsenoside Rb1 protects from Staphylococcus aureus-induced oxidative damage and apoptosis through endoplasmic reticulum-stress and death receptor-mediated pathways

2021 ◽  
Vol 219 ◽  
pp. 112353
Author(s):  
Aftab Shaukat ◽  
Irfan Shaukat ◽  
Shahid Ali Rajput ◽  
Rizwan Shukat ◽  
Sana Hanif ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Oxidative Damage ◽  
Death Receptor ◽  
Ginsenoside Rb1

scholarly journals Bottom-up proteomics analysis of the secretome of murine islets of Langerhans in elevated glucose levels

The Analyst ◽  
2017 ◽  
Vol 142 (2) ◽  
pp. 284-291 ◽  
Author(s):  
Andrew Schmudlach ◽  
Jeremy Felton ◽  
Robert T. Kennedy ◽  
Norman J. Dovichi
Keyword(s):  
Type 2 Diabetes ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Oxidative Damage ◽  
Islets Of Langerhans ◽  
High Glucose ◽  
Proteomics Analysis ◽  
Glucose Levels ◽  
Elevated Glucose

Glucotoxicity is a causative agent of type-2 diabetes, where high glucose levels damage the islets of Langerhans resulting in oxidative damage and endoplasmic reticulum stress.

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 Sulphureuine B, a drimane type sesquiterpenoid isolated from Laetiporus sulphureus induces apoptosis in glioma cells

2015 ◽  
Vol 10 (4) ◽  
pp. 844 ◽  
Author(s):  
Jing-Wei Zhang ◽  
Gong-Ling Wen ◽  
Lei Zhang ◽  
Dong-Mei Duan ◽  
Zhong-Hai Ren
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathways ◽  
Death Receptor ◽  
Glioma Cells ◽  
Edible Mushroom ◽  
Caspase 8 ◽  
Laetiporus Sulphureus ◽  
Death Receptor Signaling ◽  
Induced Apoptosis

<p class="Abstract">A drimane type sesquiterpenoids, sulphureuine B was isolated from the edible mushroom <em>Laetiporus sulphureus</em> and its antiproliferative properties were investigated using U-87MG glioma cells. It was observed that sulphu-reuine B-induced apoptosis in U-87MG cells and the mechanisms involved are endoplasmic reticulum stress, mitochondrial and death receptor mediated pathways. Endoplasmic reticulum stress was identified from the results of enormous cytoplasmic vacuolation, CHOP elevation and caspase-12 cleavage. Further, we found that treatment of sulphureuine B-induced PERK, IRE1α, and ATF6α activations. In addition, sulphureuine B-induced Bcl-2 down-regulation, cleavage of PARP, and caspase-8 activation were also affected. All these experimental results clearly revealed that sulphureuine B-induced apoptosis mediated through endoplasmic reticulum stress, mitochondrial, and death receptor signaling pathways.</p><p> </p>

scholarly journals Diet-Induced Obesity Mice Execute Pulmonary Cell Apoptosis via Death Receptor and ER-Stress Pathways after E. coli Infection

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Fengyuan Wang ◽  
Zhicai Zuo ◽  
Kejie Chen ◽  
Jing Fang ◽  
Hengmin Cui ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
High Fat Diet ◽  
Death Receptor ◽  
Apoptotic Pathway ◽  
E Coli ◽  
Diet Induced Obesity ◽  
Protein Expressions ◽  
Acute Pneumonia

Obesity has developed into a considerable health problem in the whole world. Escherichia coli (E. coli) can cause nosocomial pneumonia and induce cell apoptosis during injury and infection. Normal (lean) and diet-induced obesity mice (DIO, fed with high-fat diet) were chosen to perform nasal instillation with E. coli to establish a nonfatal acute pneumonia model. At 0 h, 12 h, 24 h, and 72 h postinfection, lung tissues were obtained to measure cell apoptosis. As shown in this study, both lean and DIO mice exhibited histopathological lesions of acute pneumonia and increased cell apoptosis in the lung infected with E. coli. Interestingly, the relative mRNA and protein expressions associated with either endoplasmic reticulum stress or death receptor apoptotic pathway were all dramatically increased in the DIO mice after infection, while only significant upregulation of death receptor apoptotic pathway in the lean mice at 72 h. These results indicated that the DIO mice executed excess cell apoptosis in the nonfatal acute pneumonia induced by E. coli infection through endoplasmic reticulum stress and death receptor apoptotic pathway.

scholarly journals CaMKII as a pathological mediator of ER stress, oxidative stress, and mitochondrial dysfunction in a murine model of nephronophthisis

2016 ◽  
Vol 310 (11) ◽  
pp. F1414-F1422 ◽  
Author(s):  
Christina Bracken ◽  
Philippe Beauverger ◽  
Olivier Duclos ◽  
Ryan J. Russo ◽  
Kelly A. Rogers ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Oxidative Damage ◽  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Cystic Kidney ◽  
Effective Inhibition ◽  
Stress Oxidative

Polycystic kidney diseases (PKDs) are genetic diseases characterized by renal cyst formation with increased cell proliferation, apoptosis, and transition to a secretory phenotype at the expense of terminal differentiation. Despite recent progress in understanding PKD pathogenesis and the emergence of potential therapies, the key molecular mechanisms promoting cystogenesis are not well understood. Here, we demonstrate that mechanisms including endoplasmic reticulum stress, oxidative damage, and compromised mitochondrial function all contribute to nephronophthisis-associated PKD. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is emerging as a critical mediator of these cellular processes. Therefore, we reasoned that pharmacological targeting of CaMKII may translate into effective inhibition of PKD in jck mice. Our data demonstrate that CaMKII is activated within cystic kidney epithelia in jck mice. Blockade of CaMKII with a selective inhibitor results in effective inhibition of PKD in jck mice. Mechanistic experiments in vitro and in vivo demonstrated that CaMKII inhibition relieves endoplasmic reticulum stress and oxidative damage and improves mitochondrial integrity and membrane potential. Taken together, our data support CaMKII inhibition as a new and effective therapeutic avenue for the treatment of cystic diseases.

Sign in / Sign up

Export Citation Format

Share Document