scholarly journals Catalase Overexpression Prevents Nuclear Factor Erythroid 2-Related Factor 2 Stimulation of Renal Angiotensinogen Gene Expression, Hypertension, and Kidney Injury in Diabetic Mice

Diabetes ◽  
2014 ◽  
Vol 63 (10) ◽  
pp. 3483-3496 ◽  
Author(s):  
S. Abdo ◽  
Y. Shi ◽  
A. Otoukesh ◽  
A. Ghosh ◽  
C.-S. Lo ◽  
...  
Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 69 ◽  
Author(s):  
Tetsuro Ishii ◽  
Eiji Warabi

Membrane-associated estrogen receptors (ER)-α36 and G protein-coupled estrogen receptor (GPER) play important roles in the estrogen’s rapid non-genomic actions including stimulation of cell proliferation. Estrogen via these receptors induces rapid activation of transcription factor nuclear factor-E2-related factor 2 (Nrf2), a master regulator of detoxification and antioxidant systems, playing a key role in the metabolic reprogramming to support cell proliferation. This review highlights the possible mechanism underlying rapid Nrf2 activation via membrane-associated estrogen receptors by estrogen and phytoestrogens. Stimulation of ER-α36-GPER signaling complex rapidly induces Src-mediated transactivation of epidermal growth factor receptor (EGFR) leading to a kinase-mediated signaling cascade. We propose a novel hypothesis that ER-α36-GPER signaling initially induces rapid and temporal activation of NADPH oxidase 1 to generate superoxide, which subsequently activates redox-sensitive neutral sphingomyelinase 2 generating the lipid signaling mediator ceramide. Generation of ceramide is required for Ras activation and ceramide-protein kinase C ζ-casein kinase 2 (CK2) signaling. Notably, CK2 enhances chaperone activity of the Cdc37-Hsp90 complex supporting activation of various signaling kinases including Src, Raf and Akt (protein kinase B). Activation of Nrf2 may be induced by cooperation of two signaling pathways, (i) Nrf2 stabilization by direct phosphorylation by CK2 and (ii) EGFR-Ras-PI 3 kinase (PI3K)-Akt axis which inhibits glycogen synthase kinase 3β leading to enhanced nuclear transport and stability of Nrf2.


2020 ◽  
Vol 30 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Juliana Saraiva dos Anjos ◽  
Ludmila Ferreira Medeiros de França Cardozo ◽  
Ana Paula Black ◽  
Greicielle Santos da Silva ◽  
Drielly Cristhiny Mendes de Vargas Reis ◽  
...  

2000 ◽  
Vol 70 (7) ◽  
pp. 1107-1110 ◽  
Author(s):  
Asher D. Schachter ◽  
Jurgen Strehlau ◽  
David Zurakowski ◽  
Lauro Vasconcellos ◽  
Yon Su Kim ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Chong Dong ◽  
Cheng Zeng ◽  
Li Du ◽  
Qian Sun

Cardiac surgery-associated acute kidney injury (AKI) is a serious and frequent complication with poor prognosis, and disruption in circadian rhythm shall adversely influence cardiovascular and renal functions via oxidative stress mechanisms. However, the role of circadian clock genes (circadian locomotor output cycle kaput (CLOCK) and brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein-1 (BMAL1)) and its interaction with nuclear factor erythroid 2-related factor 2 (Nrf2) in AKI following myocardial ischemia-reperfusion (MIR) in the diabetic rat has not yet been explored. In this study, rats were divided into the sham (S) group, MIR (M) group, diabetic (D) group, and diabetic+MIR (DM) group. At light (zeitgeber time (ZT) 0) and dark time points (ZT12), rat MIR model was established by occlusion of the left anterior descending coronary artery for 30 min followed by 2 -hour reperfusion, and then renal injury was evaluated. The renal histological changes in the DM group were significantly high compared to other groups; serum creatinine, blood urea nitrogen, and neutrophil gelatinase-associated lipocalin levels, as well as malondialdehyde and 8-iso-prostaglandin-F2α levels in renal tissues of M ZT12 and DM ZT12 subgroups, were significantly higher than those of M ZT0 and DM ZT0 subgroups, individually indicating increased oxidative stress at a dark cycle. Further, Nrf2 protein accumulated in a circadian manner with decreasing levels at night in the DM and M groups. In conclusion, renal injury following MIR was exacerbated in the diabetic rat at night through molecular mechanisms involving transcriptional control of the circadian clock on light-dark activation of Nrf2.


Sign in / Sign up

Export Citation Format

Share Document