scholarly journals BAY 11-7085 induces glucocorticoid receptor activation and autophagy that collaborate with apoptosis to induce human synovial fibroblast cell death

Oncotarget ◽  
2016 ◽  
Vol 7 (17) ◽  
pp. 23370-23382 ◽  
Author(s):  
Biserka Relic ◽  
Edith Charlier ◽  
Celine Deroyer ◽  
Olivier Malaise ◽  
Sophie Neuville ◽  
...  
Keyword(s):  
Cell Death ◽  
Glucocorticoid Receptor ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Receptor Activation ◽  
Human Synovial Fibroblast

The inhibitory effect of Aconiti Sinomontani Radix extracts on the proliferation and migration of human synovial fibroblast cell line SW982

2018 ◽  
Vol 213 ◽  
pp. 321-327
Author(s):  
Xue Deng ◽  
Lu-Ping Zheng ◽  
Zhen-Qiang Mu ◽  
Rui Lai ◽  
Guo-Ping Niu ◽  
...  
Keyword(s):  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Inhibitory Effect ◽  
Fibroblast Cell Line ◽  
Human Synovial Fibroblast ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Correction: Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (6) ◽  
pp. 2341-2341 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose G. Fernández-Bolaños ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Human Synovial Fibroblast ◽  
And Oxidative Stress

Correction for ‘Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982’ by Maria Luisa Castejón, et al., Food Funct., 2017, DOI: 10.1039/c7fo00210f.

scholarly journals Glucocorticoid receptor activation inhibits chemotherapy-induced cell death in high-grade serous ovarian carcinoma

2015 ◽  
Vol 138 (3) ◽  
pp. 656-662 ◽  
Author(s):  
Erica M. Stringer-Reasor ◽  
Gabrielle M. Baker ◽  
Maxwell N. Skor ◽  
Masha Kocherginsky ◽  
Ernst Lengyel ◽  
...  
Keyword(s):  
Cell Death ◽  
Glucocorticoid Receptor ◽  
Ovarian Carcinoma ◽  
Receptor Activation ◽  
High Grade ◽  
Serous Ovarian Carcinoma

scholarly journals Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer’s Disease Pathological Characteristics in a Transgenic Mouse Model

2020 ◽  
Vol 13 (10) ◽  
pp. 288
Author(s):  
Marielza Andrade Nunes ◽  
Mariana Toricelli ◽  
Natalia Mendes Schöwe ◽  
Helena Nascimento Malerba ◽  
Karis Ester Dong-Creste ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Functional Disability ◽  
Therapeutic Option ◽  
Receptor Activation ◽  
Hippocampal Culture ◽  
Kinin System ◽  
Organotypic Hippocampal Culture ◽  
Kallikrein Kinin System

Background: Alzheimer’s disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even death. Our group has demonstrated changes in the kallikrein–kinin system (KKS) in Alzheimer’s disease (AD) experimental models, but there is a lack of evidence about the role of the KKS in Alzheimer’s disease. Aim: In order to answer this question, we evaluated the potential of the kinin B2 receptors (BKB2R) to modify AD characteristics, particularly memory impairment, neurodegeneration, and Aβ peptide deposition. Methods: To assess the effects of B2, we used transgenic Alzheimer’s disease mice treated with B2 receptor (B2R) agonists and antagonists, and performed behavioral and biochemical tests. In addition, we performed organotypic hippocampal culture of wild-type (WT) and transgenic (TG) animals, where the density of cytokines, neurotrophin BDNF, activated astrocyte marker S100B, and cell death were analyzed after treatments. Results: Treatment with the B2R agonist preserved the spatial memory of transgenic mice and decreased amyloid plaque deposition. In organotypic hippocampal culture, treatment with B2R agonist decreased cell death, neuroinflammation, and S100B levels, and increased BDNF release. Conclusions: Our results indicate that the kallikrein–kinin system plays a beneficial role in Alzheimer’s disease through B2R activation. The use of B2R agonists could, therefore, be a possible therapeutic option for patients diagnosed with Alzheimer’s disease.

scholarly journals Inhibition of Replication Induces Non-Apoptotic Cell Death in Fibroblast Cell Lines Derived from LEC Rats

2003 ◽  
Vol 65 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Masanobu HAYASHI ◽  
Taku HAMASU ◽  
Daiji ENDOH ◽  
Reiko SHIMOJIMA ◽  
Toyo OKUI
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Fibroblast Cell ◽  
Apoptotic Cell Death ◽  
Lec Rats ◽  
Fibroblast Cell Lines

Glucocorticoid receptor activation in isolated perfused rat hearts

1989 ◽  
Vol 256 (2) ◽  
pp. C219-C225 ◽  
Author(s):  
S. M. Czerwinski ◽  
E. E. McKee ◽  
R. C. Hickson
Keyword(s):  
Glucocorticoid Receptor ◽  
Triamcinolone Acetonide ◽  
Deae Cellulose ◽  
Potassium Phosphate ◽  
Receptor Activation ◽  
Receptor Complexes ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Cellulose Binding ◽  
Isolated Perfused Rat Hearts

The formation of unactivated and activated glucocorticoid receptor complexes was studied in intact, isolated, perfused rat hearts in the presence of [3H]triamcinolone acetonide. Receptor activation, as quantified by the DNA-cellulose-binding assay, began to increase within 30 s of perfusion and reached a final steady-state level (t 1/2 = 4.6 min) with 46% of the steroid-receptor complexes bound to DNA-cellulose. With the use of a linear potassium phosphate (KP) gradient (5-400 mM), unactivated receptors eluted from DEAE-cellulose anion exchange columns at approximately 250 mM KP. Two activated receptor forms appeared, which eluted either in the wash fraction (binder IB) or between 50 and 100 mM KP (binder II) and occurred with half times of 1.3 and 2.7 min, respectively. Postperfusion cytosol preparation did not markedly influence the results as receptor binding was reduced by 10% or less when a 100-fold excess of unlabeled triamcinolone acetonide was included in the homogenizing buffer. We conclude from these results that glucocorticoids are able to exert a direct effect on the heart through binding to their own receptor in the absence of endogenous hormones. The time dependency of receptor activation supports a physiological role for this process. However, activation rates, determined from conformational changes associated with altered DEAE-cellulose elution profiles and appearance of activated receptor forms, occur earlier and may not be coordinated with the rate of activation as quantified by DNA-cellulose binding.

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