scholarly journals Reactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 Interferon Signature

2014 ◽  
Vol 21 (16) ◽  
pp. 2231-2245 ◽  
Author(s):  
Tiina Kelkka ◽  
Deborah Kienhöfer ◽  
Markus Hoffmann ◽  
Marjo Linja ◽  
Kajsa Wing ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Interferon Signature ◽  
Type 1 Interferon

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

scholarly journals Rejuvenation of mesenchymal stem cells by extracellular vesicles inhibits the elevation of reactive oxygen species

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vuong Cat Khanh ◽  
Toshiharu Yamashita ◽  
Kinuko Ohneda ◽  
Chiho Tokunaga ◽  
Hideyuki Kato ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Cellular Senescence ◽  
Skin Flap ◽  
Reactive Oxygen ◽  
Oxygen Species

Abstract Aging induces numerous cellular disorders, such as the elevation of reactive oxygen species (ROS), in a number type of cells, including mesenchymal stem cells (MSCs). However, the correlation of ROS and impaired healing abilities as well as whether or not the inhibition of elevating ROS results in the rejuvenation of elderly MSCs is unclear. The rejuvenation of aged MSCs has thus recently received attention in the field of regenerative medicine. Specifically, extracellular vesicles (EVs) act as a novel tool for stem cell rejuvenation due to their gene transfer ability with systemic effects and safety. In the present study, we examined the roles of aging-associated ROS in the function and rejuvenation of elderly MSCs by infant EVs. The data clearly showed that elderly MSCs exhibited the downregulation of superoxide dismutase (SOD)1 and SOD3, which resulted in the elevation of ROS and downregulation of the MEK/ERK pathways, which are involved in the impairment of the MSCs’ ability to decrease necrotic area in the skin flap model. Furthermore, treatment with the antioxidant Edaravone or co-overexpression of SOD1 and SOD3 rescued elderly MSCs from the elevation of ROS and cellular senescence, thereby improving their functions. Of note, infant MSC-derived EVs rejuvenated elderly MSCs by inhibiting ROS production and the acceleration of cellular senescence and promoting the proliferation and in vivo functions in both type 1 and type 2 diabetic mice.

scholarly journals Reactive Oxygen Species–Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor mRNA by Angiotensin II

Hypertension ◽  
2001 ◽  
Vol 37 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Tomotake Tokunou ◽  
Yuko Funakoshi ◽  
Kiyoko Ito ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Receptor Mrna

scholarly journals Loss of Bradykinin Signaling Does Not Accelerate the Development of Cardiac Dysfunction in Type 1 Diabetic Akita Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (8) ◽  
pp. 3536-3542 ◽  
Author(s):  
Adam R. Wende ◽  
Jamie Soto ◽  
Curtis D. Olsen ◽  
Karla M. P. Pires ◽  
John C. Schell ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Reactive Oxygen ◽  
Left Ventricular ◽  
Oxygen Species ◽  
Receptor Signaling ◽  
Genetic Ablation ◽  
Akita Mice

Bradykinin signaling has been proposed to play either protective or deleterious roles in the development of cardiac dysfunction in response to various pathological stimuli. To further define the role of bradykinin signaling in the diabetic heart, we examined cardiac function in mice with genetic ablation of both bradykinin B1 and B2 receptors (B1RB2R−/−) in the context of the Akita model of insulin-deficient type 1 diabetes (Ins2Akita/+). In 5-month-old diabetic and nondiabetic, wild-type and B1RB2R−/− mice, in vivo cardiac contractile function was determined by left-ventricular (LV) catheterization and echocardiography. Reactive oxygen species levels were measured by 2′-7′-dichlorofluorescein diacetate fluorescence. Mitochondrial function and ATP synthesis were determined in saponin-permeabilized cardiac fibers. LV systolic pressure and the peak rate of LV pressure rise and decline were decreased with diabetes but did not deteriorate further with loss of bradykinin signaling. Wall thinning and reduced ejection fractions in Akita mouse hearts were partially attenuated by B1RB2R deficiency, although other parameters of LV function were unaffected. Loss of bradykinin signaling did not increase fibrosis in Ins2Akita/+ diabetic mouse hearts. Mitochondrial dysfunction was not exacerbated by B1RB2R deficiency, nor was there any additional increase in tissue levels of reactive oxygen species. Thus, loss of bradykinin B2 receptor signaling does not abrogate the previously reported beneficial effect of inhibition of B1 receptor signaling. In conclusion, complete loss of bradykinin expression does not worsen cardiac function or increase myocardial fibrosis in diabetes.

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