scholarly journals Metallothionein and Catalase Sensitize to Diabetes in Nonobese Diabetic Mice: Reactive Oxygen Species May Have a Protective Role in Pancreatic  -Cells

Diabetes ◽  
2006 ◽  
Vol 55 (6) ◽  
pp. 1592-1604 ◽  
Author(s):  
X. Li ◽  
H. Chen ◽  
P. N. Epstein
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Nonobese Diabetic ◽  
Pancreatic Cells ◽  
Nonobese Diabetic Mice

Abstract 097: Recombinant Human Erythropoietin Prevents Reactive Oxygen Species - Induced Apoptosis Via Akt and p38 MAPK Pathway During Hypoxia/ Reperfusion Injury

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Asiya Parvin Allaudeen ◽  
Ajay Devendran ◽  
John E Baker ◽  
Anuradha Dhanasekaran
Keyword(s):  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Intact Cell ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Human Erythropoietin ◽  
In Cells

Erythropoietin (EPO) is a cytokine produced primarily in the kidney that is essential for red blood cell production. Apart from playing a role in hematopoiesis, EPO also has a protective role in heart myocytes, ovarian, glial cells brain and retinal diseases. In this study we observed that recombinant human EPO (rhEPO) reduces Hypoxia/ Reperfusion (H/R) injury by virtue of its effect on EPO receptor prosurvival signaling pathway, which ultimately leads to reduced expression of apoptotic proteins and increased survival of cardiomyocytes. H9C2 cells were exposed to H/R with or without pretreatment using 10, 15 and 20 U/ml of rhEPO. We determined viability using MTT, nuclear fragmentation by Hoechst staining, apoptotic nuclei by Acridine orange and Ethidium bromide, Reactive Oxygen Species (ROS) by Dicholorofluoresin Diacetate and activity of late apoptotic protease, Caspase-3 by colorimetric Caspase-3 assay. The expression of mitochondrial superoxide dismutase (MnSOD) by RT-PCR and Western blot, phospho-Akt and p38 MAPK by Confocal microscopy were analyzed. Cell viability is increased in cells pretreated with rhEPO compared to cell exposed to H/R. Cells subjected to H/R showed early apoptotic and late apoptotic cells but showed normal nuclei with intact cell membrane in cells pretreated with rhEPO. Intracellular production of ROS and Caspase-3 activity was decreased in cells pretreated with rhEPO compared to cells exposed to H/R. The expression of MnSOD RNA and protein was up-regulated in response to rhEPO, but not in H/R. The phosphorylative activation of Akt, p38MAPK progressively diminished during H/R but increased in rhEPO pretreated cells. We show that rhEPO prevents apoptosis in cardiomyocytes, subjected to H/R injury via phosphorylation of Akt and p38MAPK. These results it is hoped would help us distinguish the cell signaling pathways involved in cardioprotection and thus would open new avenues in cardiovascular therapy.

scholarly journals Protective Role of Programmed Death 1 Ligand 1 (PD-L1)in Nonobese Diabetic Mice: The Paradox in Transgenic Models

Diabetes ◽  
2008 ◽  
Vol 57 (7) ◽  
pp. 1861-1869 ◽  
Author(s):  
C.-J. Wang ◽  
F.-C. Chou ◽  
C.-H. Chu ◽  
J.-C. Wu ◽  
S.-H. Lin ◽  
...  
Keyword(s):  
Protective Role ◽  
Diabetic Mice ◽  
Transgenic Models ◽  
Nonobese Diabetic ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Nonobese Diabetic Mice

Abstract 070: Canonical Wnt Signaling Mediates Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility in Diabetic Mice

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
En Yin Lai ◽  
Suping Zhang ◽  
Qian Huang ◽  
Qiaoling Wang ◽  
Liang Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wnt Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Canonical Wnt Signaling ◽  
Protein Expressions ◽  
Afferent Arterioles ◽  
Gsk 3Β ◽  
Canonical Wnt

Background: Canonical Wnt signaling is involved in oxidative stress and diabetes but its role in diabetic renal microvascular dysfunction is unclear. We tested the hypothesis that enhanced canonical Wnt signaling in renal afferent arterioles from diabetic mice increases reactive oxygen species (ROS) and contractions to endothelin-1 (ET-1). Methods: Diabetic or control C57Bl/6 mice received vehicle or sulindac (40 mg·kg -1 ·day -1 ) to block canonical Wnt signaling for 4 weeks. ET-1 contractions were measured in diameter changes and H 2 O 2 and O 2 .- by fluorescence microscopy. Arteriolar protein expression and enzymatic activity were examined by standard methods. Results: Compared to control, diabetic mouse afferent arteriole had significantly increased O 2 .- (+84%) and H 2 O 2 (+91%) and enhanced sensitivity to ET-1 at 10 -8 mol·l -1 (-72±4% versus -43±4%, P<0.05) accompanied by significantly (P<0.005) reduced protein expressions and activities for catalase and superoxide dismutase 2 (SOD2). Incubation of afferent arterioles from normal or diabetic mice with PEG-SOD reduced responses to ET-1 whereas incubation with PEG-catalase reduced sensitivity to ET-1 selectively in arterioles from diabetic mice. The arteriolar protein expressions for canonical Wnt signaling indicated overactivation of this pathway in diabetic mice (2.6-fold increase in p-GSK-3β/GSK-3β and 3.3-fold decrease in p-β-catenin/β-catenin). Sulindac given to diabetic mice normalized the canonical Wnt signaling protein and arteriolar O 2 .- , H 2 O 2 and ET-1 contractions while doubling (P<0.05) microvascular catalase and SOD2. Conclusions: Increased ROS, notably H 2 O 2 , mediated by canonical Wnt signaling contributes to enhanced afferent arteriolar sensitivity to ET-1 in diabetes. Thus, antioxidant pharmacological strategies targeting canonical Wnt signaling may improve vascular function in diabetic nephropathy.

Aspirin-triggered lipoxin A4 blocks reactive oxygen species generation in endothelial cells: A novel antioxidative mechanism

2007 ◽  
Vol 97 (01) ◽  
pp. 88-98 ◽  
Author(s):  
Christina Barja-Fidalgo ◽  
Vany Nascimento-Silva ◽  
Maria Arruda ◽  
Iolanda Fierro
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Ros Generation ◽  
Oxygen Species ◽  
Lipoxin A4 ◽  
Pre Treatment

SummaryLipoxins and their aspirin-triggered carbon-15 epimers have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on cardiovascular diseases such as hypertension, atherosclerosis, and heart failure has not been investigated. One of the major features shared by these pathological conditions is the increased production of reactive oxygen species (ROS) generated by vascular NAD(P)H oxidase activation. In this study, we have examined whether an aspirin-triggered lipoxin A4 analog (ATL-1) modulates ROS generation in endothelial cells (EC). Pre-treatment of EC with ATL-1 (1–100 nM) completely blocked ROS production triggered by different agents, as assessed by dihydrorhodamine 123 and hydroethidine. Furthermore, ATL-1 inhibited the phosphorylation and translocation of the cytosplamic NAD(P)H oxidase subunit p47phox to the cell membrane as well as NAD(P)H oxidase activity. Western blot and immunofluorescence microscopy analyses showed that ATL-1 (100 nM) impaired the redox-sensitive activation of the transcriptional factor NF-κB, a critical step in several events associated to vascular pathologies. These results demonstrate that ATL-1 suppresses NAD(P)H oxidase-mediated ROS generation in EC, strongly indicating that lipoxins may play a protective role against the development and progression of cardiovascular diseases.

Protective role of carbon dioxide (CO2) in generation of reactive oxygen species

2015 ◽  
Vol 411 (1-2) ◽  
pp. 317-330 ◽  
Author(s):  
Sergey Bolevich ◽  
Alekandr Haritonovic Kogan ◽  
Vladimir Zivkovic ◽  
Dusan Djuric ◽  
Aleksey Aleksejevic Novikov ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Carbon Dioxide Co2

scholarly journals Sprr2f protects against renal injury by decreasing the level of reactive oxygen species in female mice

2020 ◽  
Vol 319 (5) ◽  
pp. F876-F884
Author(s):  
Kieu My Huynh ◽  
Anny Chuu-Yun Wong ◽  
Bo Wu ◽  
Marc Horschman ◽  
Hongjuan Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Renal Injury ◽  
Renal Damage ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Rich Region ◽  
Female Mice ◽  
Proline Rich Region

Renal injury leads to chronic kidney disease, with which women are not only more likely to be diagnosed than men but have poorer outcomes as well. We have previously shown that expression of small proline-rich region 2f ( Sprr2f), a member of the small proline-rich region ( Sprr) gene family, is increased several hundredfold after renal injury using a unilateral ureteral obstruction (UUO) mouse model. To better understand the role of Sprr2f in renal injury, we generated a Sprr2f knockout ( Sprr2f-KO) mouse model using CRISPR-Cas9 technology. Sprr2f-KO female mice showed greater renal damage after UUO compared with wild-type ( Sprr2f-WT) animals, as evidenced by higher hydroxyproline levels and denser collagen staining, indicating a protective role of Sprr2f during renal injury. Gene expression profiling by RNA sequencing identified 162 genes whose expression levels were significantly different between day 0 and day 5 after UUO in Sprr2f-KO mice. Of the 162 genes, 121 genes were upregulated after UUO and enriched with those involved in oxidation-reduction, a phenomenon not observed in Sprr2f-WT animals, suggesting a protective role of Sprr2f in UUO through defense against oxidative damage. Consistently, bilateral ischemia-reperfusion injury resulted in higher serum blood urea nitrogen levels and higher tissue reactive oxygen species in Sprr2f-KO compared with Sprr2f-WT female mice. Moreover, cultured renal epithelial cells from Sprr2f-KO female mice showed lower viability after oxidative damage induced by menadione compared with Sprr2f-WT cells that could be rescued by supplementation with reduced glutathione, suggesting that Sprr2f induction after renal damage acts as a defense against reactive oxygen species.

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