Halobenzoquinone-Induced Alteration of Gene Expression Associated with Oxidative Stress Signaling Pathways

2018 ◽  
Vol 52 (11) ◽  
pp. 6576-6584 ◽  
Author(s):  
Jinhua Li ◽  
Birget Moe ◽  
Yanming Liu ◽  
Xing-Fang Li
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Signaling Pathways ◽  
Stress Signaling

Integration of stress signals by homeodomain interacting protein kinases

2014 ◽  
Vol 395 (4) ◽  
pp. 375-386 ◽  
Author(s):  
Michael Lienhard Schmitz ◽  
Alfonso Rodriguez-Gil ◽  
Juliane Hornung
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Protein Kinases ◽  
Metabolic Stress ◽  
Stress Signaling ◽  
Oxygen Intermediates ◽  
Interacting Protein ◽  
Downstream Effector ◽  
Stress Signals ◽  
Effector Pathways

Abstract The family of homeodomain interacting protein kinases (HIPKs) consists of four related kinases, HIPK1 to HIPK4. These serine/threonine kinases are evolutionary conserved and derive from the yeast kinase Yak1. The largest group of HIPK phosphorylation substrates is represented by transcription factors and chromatin-associated regulators of gene expression, thus transferring HIPK-derived signals into changes of gene expression programs. The HIPKs mainly function as regulators of developmental processes and as integrators of a wide variety of stress signals. A number of conditions representing precarious situations, such as DNA damage, hypoxia, reactive oxygen intermediates and metabolic stress affect the function of HIPKs. The kinases function as integrators for these stress signals and feed them into many different downstream effector pathways that serve to cope with these precarious situations. HIPKs do not function as essential core components in the different stress signaling pathways, but rather serve as modulators of signal output and as connectors of different stress signaling pathways. Their central role as signaling hubs with the ability to shape many downstream effector pathways frequently implies them in proliferative diseases such as cancer or fibrosis.

Vitamin E synthetic derivate—TPGS—selectively induces apoptosis in jurkat t cells via oxidative stress signaling pathways: implications for acute lymphoblastic leukemia

APOPTOSIS ◽  
2016 ◽  
Vol 21 (9) ◽  
pp. 1019-1032 ◽  
Author(s):  
Cristian Ruiz-Moreno ◽  
Marlene Jimenez-Del-Rio ◽  
Ligia Sierra-Garcia ◽  
Betty Lopez-Osorio ◽  
Carlos Velez-Pardo
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Vitamin E ◽  
Acute Lymphoblastic Leukemia ◽  
Signaling Pathways ◽  
Lymphoblastic Leukemia ◽  
Stress Signaling ◽  
Jurkat T Cells

Abstract 12423: Normoxic Therapy Attenuated Oxidative Stress Related mRNA Gene Expressions in a Post-Cardiac Arrest Rat Model

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Tomoaki Aoki ◽  
Koichiro Shinozaki ◽  
Yu Okuma ◽  
Kei Hayashida ◽  
Ryosuke Takegawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cardiac Arrest ◽  
Signaling Pathways ◽  
Expression Patterns ◽  
Expression Levels ◽  
Mrna Gene ◽  
The Brain ◽  
Mrna Gene Expression ◽  
Gene Expression Levels

Objective: We recently reported that post-resuscitation normoxic therapy attenuates oxidative stress in multiple organs and improves post-cardiac arrest (CA) organ injury, oxygen metabolism, and survival. Yet, detailed mechanisms of gene expression patterns and signaling pathways mitigated by normoxic therapy have not been elucidated. Therefore, we assessed post-resuscitation normoxic therapy-modified gene expression of oxidative stress-related signaling molecules. Methods: Rats were resuscitated from 10 minutes of asphyxial CA and divided into 2 groups: those that inhaled 100% supplemental O 2 (CA-FIO2 1.0) and those that inhaled 30% supplemental O 2 (CA-FIO2 0.3). Control groups were also prepared for comparison (control-FIO2 1.0, control-FIO2 0.3). At 2 hours after resuscitation, brain and heart tissues were collected, and mRNA purifications followed by real-time PCR measurements were performed to compare gene expression of hyperoxia-induced inflammatory and apoptosis-related signaling pathways amongst these groups. Results: In the brain, relative IL-1 beta mRNA gene expression levels, which represent inflammatory signaling pathways, increased post-CA (8.1±2.3 in CA-FIO2 1.0 and 1.0±0.4 in control-FIO2 0.3, p<0.05), but were significantly attenuated by normoxic therapy (2.3±0.2 in CA-FIO2 0.3, p<0.05). Likewise, normoxic therapy significantly reduced oxidative stress-induced inflammatory (NFKB1, TGFB1, MAPK14, TRAF6) and apoptosis-related (BAX, EGF) mRNA gene expression levels in the brain, whereas no statistical differences were detected in the heart. Conclusions: Post-CA normoxic therapy significantly attenuated the gene expression of oxidative stress-induced inflammation and apoptosis in the brain, while there were no remarkable changes in the heart. Therefore, it is inferred that the heart is more tolerant to hyperoxic injury compared to the brain.

Acute lysine overload provokes marked striatum injury involving oxidative stress signaling pathways in glutaryl-CoA dehydrogenase deficient mice

2019 ◽  
Vol 129 ◽  
pp. 104467 ◽  
Author(s):  
Alexandre Umpierrez Amaral ◽  
Bianca Seminotti ◽  
Janaína Camacho da Silva ◽  
Francine Hehn de Oliveira ◽  
Rafael Teixeira Ribeiro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Stress Signaling ◽  
Deficient Mice
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