27. mt-Nd2c Increases Susceptibility to Type 1 Diabetes (T1D) by Increasing Mitochondrial Reactive Oxygen Species (ROS) Production

Mitochondrion ◽  
2009 ◽  
Vol 9 (1) ◽  
pp. 67-68
Author(s):  
Aaron M. Gusdon ◽  
Jing Chen ◽  
Clayton E. Mathews
Keyword(s):  
Reactive Oxygen Species ◽  
Type 1 Diabetes ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals Mitochondrial Reactive Oxygen Species and Type 1 Diabetes

2018 ◽  
Vol 29 (14) ◽  
pp. 1361-1372 ◽  
Author(s):  
Jing Chen ◽  
Scott E. Stimpson ◽  
Gabriel A. Fernandez-Bueno ◽  
Clayton E. Mathews
Keyword(s):  
Reactive Oxygen Species ◽  
Type 1 Diabetes ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals NADPH Oxidase-Derived Overproduction of Reactive Oxygen Species Impairs Postischemic Neovascularization in Mice with Type 1 Diabetes

2006 ◽  
Vol 169 (2) ◽  
pp. 719-728 ◽  
Author(s):  
Téni G Ebrahimian ◽  
Christophe Heymes ◽  
Dong You ◽  
Olivier Blanc-Brude ◽  
Barend Mees ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Type 1 Diabetes ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species

Reactive Oxygen Species Damaged Hemoglobin Presents Unique Epitopes for Type 1 Diabetes Autoantibodies

2007 ◽  
Vol 2 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Zafar Rasheed ◽  
Rizwan Ahmad ◽  
Naila Rasheed ◽  
Trivendra Tripathi ◽  
Rashid Ali
Keyword(s):  
Reactive Oxygen Species ◽  
Type 1 Diabetes ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetes Autoantibodies

scholarly journals Survival Signaling by C-RAF: Mitochondrial Reactive Oxygen Species and Ca2+ Are Critical Targets

2008 ◽  
Vol 28 (7) ◽  
pp. 2304-2313 ◽  
Author(s):  
Andrey V. Kuznetsov ◽  
Julija Smigelskaite ◽  
Christine Doblander ◽  
Manickam Janakiraman ◽  
Martin Hermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Mitochondrial Ros ◽  
Survival Signaling ◽  
First Time

ABSTRACT Survival signaling by RAF occurs through largely unknown mechanisms. Here we provide evidence for the first time that RAF controls cell survival by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and Ca2+. Interleukin-3 (IL-3) withdrawal from 32D cells resulted in ROS production, which was suppressed by activated C-RAF. Oncogenic C-RAF decreased the percentage of apoptotic cells following treatment with staurosporine or the oxidative stress-inducing agent tert-butyl hydroperoxide. However, it was also the case that in parental 32D cells growing in the presence of IL-3, inhibition of RAF signaling resulted in elevated mitochondrial ROS and Ca2+ levels. Cell death is preceded by a ROS-dependent increase in mitochondrial Ca2+, which was absent from cells expressing transforming C-RAF. Prevention of mitochondrial Ca2+ overload after IL-3 deprivation increased cell viability. MEK was essential for the mitochondrial effects of RAF. In summary, our data show that survival control by C-RAF involves controlling ROS production, which otherwise perturbs mitochondrial Ca2+ homeostasis.

scholarly journals The role of reactive oxygen species and proinflammatory cytokines in type 1 diabetes pathogenesis

2013 ◽  
Vol 1281 (1) ◽  
pp. 16-35 ◽  
Author(s):  
Lindsey E. Padgett ◽  
Katarzyna A. Broniowska ◽  
Polly A. Hansen ◽  
John A. Corbett ◽  
Hubert M. Tse
Keyword(s):  
Reactive Oxygen Species ◽  
Type 1 Diabetes ◽  
Proinflammatory Cytokines ◽  
Reactive Oxygen ◽  
Oxygen Species
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