scholarly journals Estradiol increases rat aorta endothelium-derived relaxing factor (EDRF) activity without changes in endothelial NO synthase gene expression: possible role of decreased endothelium-derived superoxide anion production

1999 ◽  
Vol 41 (3) ◽  
pp. 672-681 ◽  
Author(s):  
M Barbacanne
Keyword(s):  
Gene Expression ◽  
Superoxide Anion ◽  
Rat Aorta ◽  
No Synthase ◽  
Superoxide Anion Production ◽  
Relaxing Factor ◽  
Endothelial No Synthase ◽  
Anion Production ◽  
Endothelium Derived Relaxing Factor

Inducible NO synthase: role in cellular signalling

1999 ◽  
Vol 202 (6) ◽  
pp. 645-653 ◽  
Author(s):  
K.F. Beck ◽  
W. Eberhardt ◽  
S. Frank ◽  
A. Huwiler ◽  
U.K. Messmer ◽  
...  
Keyword(s):  
Gene Expression ◽  
No Synthase ◽  
Signalling Pathways ◽  
Target Cells ◽  
Activated Macrophages ◽  
The Past ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Intercellular Messenger

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of neurotransmitter. In 1992, Science picked NO as the ‘Molecule of the Year’, and over the past years NO has become established as a universal intercellular messenger that acutely affects important signalling pathways and, on a more long-term scale, modulates gene expression in target cells. These actions will form the focus of the present review.

scholarly journals Role of TSPO/VDAC1 Upregulation and Matrix Metalloproteinase-2 Localization in the Dysfunctional Myocardium of Hyperglycaemic Rats

2020 ◽  
Vol 21 (20) ◽  
pp. 7432 ◽  
Author(s):  
Micaela Gliozzi ◽  
Federica Scarano ◽  
Vincenzo Musolino ◽  
Cristina Carresi ◽  
Miriam Scicchitano ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Nadph Oxidase ◽  
Diabetic Cardiomyopathy ◽  
Superoxide Anion ◽  
Matrix Metalloproteinase 2 ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Voltage Dependent ◽  
Selective Channel

Clinical management of diabetic cardiomyopathy represents an unmet need owing to insufficient knowledge about the molecular mechanisms underlying the dysfunctional heart. The aim of this work is to better clarify the role of matrix metalloproteinase 2 (MMP-2) isoforms and of translocator protein (TSPO)/voltage-dependent anion-selective channel 1 (VDAC1) modulation in the development of hyperglycaemia-induced myocardial injury. Hyperglycaemia was induced in Sprague-Dawley rats through a streptozocin injection (35 mg/Kg, i.p.). After 60 days, cardiac function was analysed by echocardiography. Nicotinamide Adenine Dinucleotide Phosphate NADPH oxidase and TSPO expression was assessed by immunohistochemistry. MMP-2 activity was detected by zymography. Superoxide anion production was estimated by MitoSOX™ staining. Voltage-dependent anion-selective channel 1 (VDAC-1), B-cell lymphoma 2 (Bcl-2), and cytochrome C expression was assessed by Western blot. Hyperglycaemic rats displayed cardiac dysfunction; this response was characterized by an overexpression of NADPH oxidase, accompanied by an increase of superoxide anion production. Under hyperglycaemia, increased expression of TSPO and VDAC1 was detected. MMP-2 downregulated activity occurred under hyperglycemia and this profile of activation was accompanied by the translocation of intracellular N-terminal truncated isoform of MMP-2 (NT-MMP-2) from mitochondria-associated membrane (MAM) into mitochondria. In the onset of diabetic cardiomyopathy, mitochondrial impairment in cardiomyocytes is characterized by the dysregulation of the different MMP-2 isoforms. This can imply the generation of a “frail” myocardial tissue unable to adapt itself to stress.

Role of nitric oxide (EDRF) in radiocontrast acute renal failure in rats

1994 ◽  
Vol 267 (3) ◽  
pp. F374-F379 ◽  
Author(s):  
D. Schwartz ◽  
M. Blum ◽  
G. Peer ◽  
Y. Wollman ◽  
A. Maree ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Therapeutic Approach ◽  
No Synthase ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Synthase Inhibitor ◽  
Novel Therapeutic

This study was undertaken to examine the possible role of endothelium-derived relaxing factor (EDRF), identified as nitric oxide (NO), in the pathogenesis of radiocontrast-induced acute renal failure in rats. Normal and salt-depleted rats were monitored for 60 min or 24 h after radiocontrast administration. The administration of L-arginine to normal rats abolished the immediate decrease in p-aminohippurate clearance (CPAH) and attenuated the decrease in inulin clearance (CIn). The administration of NO synthase inhibitor to the salt-depleted animals resulted in a significantly more pronounced decrease in CPAH compared with both the control and the L-arginine-treated animals. The recovery of CIn 24 h after radiocontrast administration to the salt-depleted rats was significantly better in the L-arginine-treated rats than in either the control or inhibitor-treated groups. The administration of radiocontrast material resulted in a significant decrease in urinary guanosine 3',5'-cyclic monophosphate as well as NO2 + NO3 excretion. This decrease was significantly attenuated by L-arginine. Our results 1) suggest that NO plays a major role in the pathogenesis of radiocontrast-induced acute renal failure and 2) suggest a novel therapeutic approach, i.e., the use of L-arginine in this form of acute renal failure.

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