Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs

Li, Huige; Wallerath, Thomas; Münzel, Thomas; Förstermann, Ulrich

doi:10.1016/s1089-8603(02)00111-8

Cited by 197 publications

(146 citation statements)

References 178 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…In the beginning of the development of atherosclerosis, there is an upregulation of eNOS expression, whereas a downregulation of eNOS expression is found in later stages (24). In the present study, we did not find any differences in the expression of eNOS in umbilical arteries from newborns born SGA and…”

Section: Isoforms Of Noscontrasting

confidence: 68%

Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age

Dellee

Tobias

et al. 2012

Pediatr Res

Self Cite

View full text Add to dashboard Cite

Background: Modified expression of nitric oxide synthases (NOss) and an imbalance between the pro-oxidative and the antioxidative system accompany endothelial dysfunction, the first stage of atherosclerosis. humans born small (sGa) or large (LGa) for gestational age are at higher risk of developing atherosclerosis later in life than humans born appropriate for gestational age (aGa). We hypothesized that indicators of endothelial dysfunction could be detectable at birth. The purpose of this study was to find out whether the expression patterns of NO synthases (endothelial NOs (eNOs), inducible NOs (iNOs), and neuronal NOs (nNOs)), pro-oxidative enzymes (components of nicotinamide adenine dinucleotide phosphate (NaDPh) oxidases, NaDPh oxidase 1 (NOX1), NOX2, NOX4, p22phox, and p47phox), and antioxidative enzymes (superoxide dismutase 1-3 (sOD1-3), glutathione peroxidase 1 (GPX1), and catalase) in umbilical arteries differ among sGa, LGa, and aGa newborns. Methods: Thirty-six umbilical cords were obtained from healthy, normal, full-term sGa, aGa, and LGa newborns. The umbilical arteries were dissected and homogenized. mRNa expression was analyzed with quantitative real-time PcR. Western blotting was performed to determine protein expression. results: mRNa and protein expression of NO synthases, prooxidative enzymes, and antioxidative enzymes did not differ in the umbilical arteries from newborns of the three groups. conclusion: Indicators of endothelial dysfunction in terms of differences in enzyme expression in sGa or LGa newborns vs. aGa newborns were not present at birth.

show abstract

Section: Isoforms Of Noscontrasting

confidence: 68%

Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age

Dellee

Tobias

et al. 2012

Pediatr Res

Self Cite

View full text Add to dashboard Cite

show abstract

“…Several studies indicated that the action of Epo in the heart is associated with activation of PI3K-Akt pathway with subsequent up-regulation of NO production (83, 160,163,164 and is known to regulate the activity of l-type calcium channels by phosphorylation and S-nitrosylation. Upon eNOS activation and NO binding to soluble guanylyl cyclase, PKG-induced phosphorylation of contractile protein machinery is induced (165).…”

Section: Epor In the Heartmentioning

confidence: 99%

Epo and Non-hematopoietic Cells: What Do We Know?

Ogunshola

Bogdanova

2013

Methods in Molecular Biology

View full text Add to dashboard Cite

“…12 Moreover, the combination of eNOS gene therapy and sildenafil results in a synergistic increase in erectile response in diabetic rats, 17 further suggesting the role of impaired NO-mediated responses. However, several studies in the diabetic penis, 11,18 and an increasing number of studies in nonpenile diabetic vascular beds 19 have shown no changes or increased protein expression of eNOS rather than its decrease, despite diminished NO production. These findings question the notion of decreased expression of eNOS in endothelial dysfunction in diabetes.…”

Section: Enos Expressionmentioning

confidence: 99%

“…The upregulation of eNOS may represent a compensatory mechanism to increase NO production. 19 Thus, ROS may contribute to the upregulation of eNOS expression seen in diabetes and other types of vascular pathophysiology.…”

Section: Enos Expressionmentioning

confidence: 99%

Endothelial dysfunction in diabetic erectile dysfunction

2006

View full text Add to dashboard Cite

Erectile dysfunction (ED) is highly prevalent in diabetes mellitus. Pathophysiological mechanisms underlying diabetes-associated ED are in large part due to endothelial dysfunction, which functionally refers to the inability of the endothelium to produce vasorelaxing messengers and to maintain vasodilation and vascular homeostasis. The precise mechanisms leading to endothelial dysfunction in the diabetic vasculature, including the penis, are not yet fully understood. Hyperglycemia affects endothelial nitric oxide synthase activity and nitric oxide production/ bioavailability, nitric oxide-independent relaxing factors, oxidative stress, production and/or action of hormones, growth factors and/or cytokines, and generation and activity of opposing vasoconstrictors. Considering recent advances in the field of vascular biology and diabetes, the emphasis in this review is placed on the mechanisms of hyperglycemia-induced endothelial dysfunction in the pathophysiology of diabetes-associated ED.

show abstract

Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs

Cited by 197 publications

References 178 publications

Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age

Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age

Epo and Non-hematopoietic Cells: What Do We Know?

Endothelial dysfunction in diabetic erectile dysfunction

Contact Info

Product

Resources

About