scholarly journals Adiponectin inhibits the generation of reactive oxygen species induced by high glucose and promotes endothelial NO synthase formation in human mesangial cells

2012 ◽  
Vol 6 (2) ◽  
pp. 449-453 ◽  
Author(s):  
FANG YUAN ◽  
YI-NING LI ◽  
YING-HONG LIU ◽  
BIN YI ◽  
JUN-WEI TIAN ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
High Glucose ◽  
Mesangial Cells ◽  
Reactive Oxygen ◽  
No Synthase ◽  
Oxygen Species ◽  
Human Mesangial Cells ◽  
Endothelial No Synthase

Phenotypic Modifications of Human Mesangial Cells by Extracellular Matrix: The Importance of Matrix in the Contractile Response to Reactive Oxygen Species

2000 ◽  
Vol 8 (2) ◽  
pp. 97-103 ◽  
Author(s):  
M. Carmen Iglesias-de la Cruz ◽  
M. Piedad Ruiz-Torres ◽  
F. Javier De Lucio-Cazaña ◽  
Manuel Rodríguez-Puyol ◽  
Diego Rodríguez-Puyol
Keyword(s):  
Reactive Oxygen Species ◽  
Extracellular Matrix ◽  
Contractile Response ◽  
Mesangial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Human Mesangial Cells

Mechanisms of homocysteine-induced oxidative stress

2005 ◽  
Vol 289 (6) ◽  
pp. H2649-H2656 ◽  
Author(s):  
Neetu Tyagi ◽  
Kara C. Sedoris ◽  
Mesia Steed ◽  
Alexander V. Ovechkin ◽  
Karni S. Moshal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
No Synthase ◽  
Oxygen Species ◽  
Neuronal No Synthase ◽  
Endothelial No Synthase ◽  
Inducible No Synthase ◽  
Cardiovascular Morbidity And Mortality

Hyperhomocysteinemia decreases vascular reactivity and is associated with cardiovascular morbidity and mortality. However, pathogenic mechanisms that increase oxidative stress by homocysteine (Hcy) are unsubstantiated. The aim of this study was to examine the molecular mechanism by which Hcy triggers oxidative stress and reduces bioavailability of nitric oxide (NO) in cardiac microvascular endothelial cells (MVEC). MVEC were cultured for 0–24 h with 0–100 μM Hcy. Differential expression of protease-activated receptors (PARs), thioredoxin, NADPH oxidase, endothelial NO synthase, inducible NO synthase, neuronal NO synthase, and dimethylarginine-dimethylaminohydrolase (DDAH) were measured by real-time quantitative RT-PCR. Reactive oxygen species were measured by using a fluorescent probe, 2′,7′-dichlorofluorescein diacetate. Levels of asymmetric dimethylarginine (ADMA) were measured by ELISA and NO levels by the Griess method in the cultured MVEC. There were no alterations in the basal NO levels with 0–100 μM Hcy and 0–24 h of treatment. However, Hcy significantly induced inducible NO synthase and decreased endothelial NO synthase without altering neuronal NO synthase levels. There was significant accumulation of ADMA, in part because of reduced DDAH expression by Hcy in MVEC. Nitrotyrosine expression was increased significantly by Hcy. The results suggest that Hcy activates PAR-4, which induces production of reactive oxygen species by increasing NADPH oxidase and decreasing thioredoxin expression and reduces NO bioavailability in cultured MVEC by 1) increasing NO2-tyrosine formation and 2) accumulating ADMA by decreasing DDAH expression.

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