scholarly journals Effect of proteasome inhibitor MG132 on the expression of oxidative metabolism related genes in tomato

2021 ◽  
Author(s):  
Burcu KARPUZ ◽  
Özgür ÇAKIR
Keyword(s):  
Oxidative Metabolism ◽  
Proteasome Inhibitor ◽  
Proteasome Inhibitor Mg132

The proteasome inhibitor MG132 induces apoptosis in human pancreatic cancer cells

2005 ◽  
Author(s):  
Moritz Wente ◽  
Guido Eibl ◽  
Howard Reber ◽  
Helmut Friess ◽  
Markus Büchler ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Proteasome Inhibitor ◽  
Human Pancreatic Cancer ◽  
Proteasome Inhibitor Mg132 ◽  
Pancreatic Cancer Cells

scholarly journals Over-Activated Proteasome Mediates Neuroinflammation on Acute Intracerebral Hemorrhage in Rats

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1326 ◽  
Author(s):  
Hock-Kean Liew ◽  
Wei-Fen Hu ◽  
Peter Bor-Chian Lin ◽  
Po-Kai Wang ◽  
Andy Po-Yi Tsai ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Er Stress ◽  
Inflammatory Cytokines ◽  
Proteasome Inhibitor ◽  
Neuronal Cell ◽  
Neurological Deficits ◽  
Critical Event ◽  
Secondary Brain Injury ◽  
Proteasome Inhibitor Mg132 ◽  
Pro Inflammatory Cytokines

Background: Neuroinflammation is a hallmark in intracerebral hemorrhage (ICH) that induces secondary brain injury, leading to neuronal cell death. ER stress-triggered apoptosis and proteostasis disruption caused neuroinflammation to play an important role in various neurological disorders. The consequences of ER stress and proteostasis disruption have rarely been studied during the course of ICH development. Methods: ICH was induced by collagenase VII-S intrastriatal infusion. Animals were sacrificed at 0, 3, 6, 24, and 72 h post-ICH. Rats were determined for body weight changes, hematoma volume, and neurological deficits. Brain tissues were harvested for molecular signaling analysis either for ELISA, immunoblotting, immunoprecipitation, RT-qPCR, protein aggregation, or for histological examination. A non-selective proteasome inhibitor, MG132, was administered into the right striatum three hours prior to ICH induction. Results: ICH-induced acute proteasome over-activation caused the early degradation of the endoplasmic reticulum (ER) chaperone GRP78 and IκB protein. These exacerbations were accompanied by the elevation of pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP) and pro-inflammatory cytokines expression via nuclear factor-kappa B (NF-κB) signal activation. Pre-treatment with proteasome inhibitor MG132 significantly ameliorated the ICH-induced ER stress/proteostasis disruption, pro-inflammatory cytokines, neuronal cells apoptosis, and neurological deficits. Conclusions: ICH induced rapid proteasome over-activation, leading to an exaggeration of the ER stress/proteostasis disruption, and neuroinflammation might be a critical event in acute ICH pathology.

Proteasome inhibitor MG132 modulates inflammatory pain by central mechanisms in adjuvant arthritis

2014 ◽  
Vol 20 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Aisha Siddiqah Ahmed ◽  
Mahmood Ahmed ◽  
Jian Li ◽  
Harvest F. Gu ◽  
Georgy Bakalkin ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Adjuvant Arthritis ◽  
Proteasome Inhibitor ◽  
Proteasome Inhibitor Mg132

scholarly journals Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons

Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1507
Author(s):  
Young Min Kim ◽  
Hyun-Jung Kim
Keyword(s):  
Cell Fate ◽  
Proteasome Inhibitor ◽  
Cell Function ◽  
B Cell Lymphoma ◽  
Proteasome Inhibition ◽  
Camp Response Element Binding ◽  
Culture Conditions ◽  
Proteasome Inhibitor Mg132 ◽  
Bdnf Expression ◽  
Protein Ratio

Regulation of protein expression is essential for maintaining normal cell function. Proteasomes play important roles in protein degradation and dysregulation of proteasomes is implicated in neurodegenerative disorders. In this study, using a proteasome inhibitor MG132, we showed that proteasome inhibition reduces neural stem cell (NSC) proliferation and is toxic to NSCs. Interestingly, MG132 treatment increased the percentage of neurons in both proliferation and differentiation culture conditions of NSCs. Proteasome inhibition reduced B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein ratio. In addition, MG132 treatment induced cAMP response element-binding protein phosphorylation and increased the expression of brain-derived neurotrophic factor transcripts and proteins. These data suggest that proteasome function is important for NSC survival and differentiation. Moreover, although MG132 is toxic to NSCs, it may increase neurogenesis. Therefore, by modifying MG132 chemical structure and developing none toxic proteasome inhibitors, neurogenic chemicals can be developed to control NSC cell fate.

scholarly journals The Proteasome Inhibitor, MG132, Attenuates Diabetic Nephropathy by Inhibiting SnoN DegradationIn VivoandIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Huang ◽  
Chen Yang ◽  
Qinling Nan ◽  
Chenlin Gao ◽  
Hong Feng ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Proteasome Inhibitor ◽  
Kidney Damage ◽  
Control Group ◽  
Glomerular Mesangial Cells ◽  
Proteasome Inhibitor Mg132 ◽  
Ubiquitin Proteasome Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway

Transforming growth factor-β(TGF-β) has been shown to be involved in diabetic nephropathy (DN). The SnoN protein can regulate TGF-βsignaling through interaction with Smad proteins. Recent studies have shown that SnoN is mainly degraded by the ubiquitin-proteasome pathway. However, the role of SnoN in the regulation of TGF-β/Smad signaling in DN is still unclear. In this study, diabetic rats were randomly divided into a diabetic control group (DC group) and a proteasome inhibitor (MG132) diabetes therapy group (DT group). Kidney damage parameters and the expression of SnoN, Smurf2, and TGF-βwere observed. Simultaneously, we cultured rat glomerular mesangial cells (GMCs) stimulated with high glucose, and SnoN and Arkadia expression were measured. Results demonstrated that 24-hour urine protein, ACR, BUN, and the expression of Smurf2 and TGF-βwere significantly increased (P<0.05), whereas SnoN was significantly decreased in the DC group (P<0.05). However, these changes diminished after treatment with MG132. SnoN expression in GMCs decreased significantly (P<0.05), but Arkadia expression gradually increased due to high glucose stimulation (P<0.05), which could be almost completely reversed by MG132 (P<0.05). The present results support the hypothesis that MG132 may alleviate kidney damage by inhibiting SnoN degradation and TGF-βactivation, suggesting that the ubiquitin-proteasome pathway may become a new therapeutic target for DN.

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