eNOS phosphorylation in health and disease

Kolluru, Gopi K.; Siamwala, Jamila H.; Chatterjee, Suvro

doi:10.1016/j.biochi.2010.03.020

Cited by 156 publications

(155 citation statements)

References 234 publications

Supporting

Mentioning

144

Contrasting

Unclassified

Order By: Relevance

“…These findings are consistent with the notion that acetylcholine mediates NO induction independent of Ser1177 phosphorylation. 34,35 In cultured microvascular endothelial cells, treatment of the cells with LMWF at 30 mg/ml caused significant augmentations in Ser1177 phosphorylation and NO production, and their maximum responses were accordingly seen in the vasoendothelial cells exposure to LMWF for at least 20 min (Figures 7d À f). These findings are consistent with the findings in LMWF-treated diabetic vessels ( Figure 5) and normal aorta (Figures 7a À c).…”

Section: Effects Of Lmwf On Enos Phosphorylation and No Production Inmentioning

confidence: 96%

“…3,7,10,11 Endothelium-derived NO is mainly generated by activation of eNOS and its phosphorylation at Ser1177. 34,35 Thus, we next investigated the levels of eNOS expression and phosphorylation at Ser1177 in vessels and NO level in rat serum by western blotting and ELISA. As shown in Figure 5, the relative levels of eNOS expression, p-eNOS at Ser1177, and the NO synthesis were significantly decreased in diabetic aorta and also in caudal arteries (data not shown) compared with those in normal arteries.…”

Section: Effects Of Lmwf On Enos Expression and No Production In Diabmentioning

confidence: 99%

See 1 more Smart Citation

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Cui

Zheng

Zhang

et al. 2014

Laboratory Investigation

View full text Add to dashboard Cite

Endothelial dysfunction, characterized by impairment of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability, has been implicated in diabetic cardiovascular pathogenesis. In this study, low-molecular-weight fucoidan (LMWF), which has multiple biological activities including anti-inflammatory and anti-oxidative properties, was investigated for its protective effect against endothelial dysfunction in Goto-Kakizaki type 2 diabetic rats. LMWF (50, 100, or 200 mg/kg/day) or probucol (100 mg/kg/day) were given to diabetic rats for 12 weeks. Basal blood pressure, acetylcholine-or flow-mediated relaxation of mesenteric and paw arteries, endothelium-dependent dilation of aorta, eNOS phosphorylation, and NO production were measured using laser Doppler flowmetry, force myograph, hematoxylin and eosin staining, western blot analysis, and an NO assay. We found that LMWF robustly ameliorated the basal hypertension and impairment of endothelium-dependent relaxation in the aorta, as well as mesenteric and paw arteries in diabetic rats. In addition, the reduction in eNOS phosphorylation at Ser1177, eNOS expression, and NO production because of diabetes were partially reversed by LMWF treatment. However, probucol, a lipid-modifying drug with antioxidant properties, displayed only mild effects. Moreover, LMWF induced, in a dose-dependent manner, endotheliumdependent vasodilation and eNOS phosphorylation at Ser1177 in normal aorta, and also promoted Ser1177 phosphorylation and NO synthesis in primary cultured vasoendothelial cells. Thus, these data demonstrate for the first time that fucoidan protects vasoendothelial function and reduces basal blood pressure in type 2 diabetes rats via, at least in part, preservation of eNOS function. Fucoidan is therefore a potential candidate drug for protection of endothelium in diabetic cardiovascular complications. KEYWORDS: diabetes; endothelium-dependent vasodilation; endothelial nitric oxide synthase; low-molecular-weight fucoidan; nitric oxide Diabetic patients are at high risk of endothelial dysfunction and vascular lesions, because of multiple harmful stimuli, such as hyperglycemia, hyperlipidemia, and oxidative stress. These patients are susceptible to atherosclerosis, hypertension, and peripheral vascular disease. 1,2 It is well established that endothelium-derived nitric oxide (NO) maintains vascular homeostasis and health through vasodilation and protection of vasculature from various damaging agents. [3][4][5] Loss of NO induces increased activity of proinflammatory transcription factors, such as nuclear factor kappa B, resulting in expression of leukocyte adhesion molecules and production of chemokines and cytokines, which further promote endothelial inflammation and atherosclerosis. 5,6 Therefore, the endothelial dysfunction caused by imbalance of NO bioavailability in early-stage diabetes has been implicated as a sign or a predictor of a future cardiovascular event. [6][7][8] Mechanistically, a disturbance in endothelial NO synthase (eNOS) activity, refe...

show abstract

Section: Effects Of Lmwf On Enos Phosphorylation and No Production Inmentioning

confidence: 96%

Section: Effects Of Lmwf On Enos Expression and No Production In Diabmentioning

confidence: 99%

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Cui

Zheng

Zhang

et al. 2014

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…The loss of eNOS function has been implicated in a number of cardiovascular diseases, including diabetes. [105][106][107][108] On the other hand, eNOS overexpression has a protective effect against chemical-induced diabetes. 108,109 The mechanisms by which eNOS protect against diabetes are not clear.…”

Section: Nitric Oxide As a Survival Molecule In Pancreatic β-Cellsmentioning

confidence: 99%

“…17,107 Cytosolic NO produced by pAkt-activated eNOS may act on TFs to inhibit their nuclear translocation and activity (e.g., Nrf2) or enhance their transcriptional properties (e.g., HIF1α). In PC12 cells, low concentrations of NO promote cytoprotection and cell survival through the activation of Nrf2.…”

Section: No Regulates Mitochondrial Permeability and Activitymentioning

confidence: 99%

Regulation of pancreatic β-cell survival by nitric oxide

Bedoya¹,

Salguero-Aranda

Cahuana

et al. 2012

Islets

View full text Add to dashboard Cite

“…Aging and an unhealthy lifestyle impair endothelial cells, which contributes to the pathogenesis of several cardiovascular diseases. This manifests in its earliest form as an attenuation of endotheliumdependent dilator responses as a consequence of the alteration in the expression or activity of endothelial nitric oxide synthases (eNOS) [2]. Endothelial nitric oxide synthases, which play a pivotal role in vasorelaxation, are derived from nitric oxide (NO) and are phosphorylated by the PI3K/Akt activating signaling pathway via the increase of shear stress at the cellular level and in isolated blood vessels [3].…”

Section: Introduction *mentioning

confidence: 99%

Resistance exercise training increase activation of AKT-eNOS and Ref-1 expression by FOXO-1 activation in aorta of F344 rats

Yoon

et al. 2015

J. Exerc. Nutr, Biochem.

View full text Add to dashboard Cite

. Resistance exercise training increase activation of AKT-eNOS and Ref-1 expression by FOXO-1 activation in aorta of F344 rats. JENB., Vol. 19, No. 3, pp.165-171, 2015 [Purpose] This study investigated the effects of resistance exercise on the Akt-eNOS, the activation of antioxidant protein and FOXO1 in the aorta of F344 rats.[Methods] Male 7 week-old F344 rats were randomly divided into 2 groups: a climbing group (n = 6) and a sedentary group (n = 6). H&E staining and western blotting were used to analyze the rat aortas and target proteins.

show abstract

eNOS phosphorylation in health and disease

Cited by 156 publications

References 234 publications

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Regulation of pancreatic β-cell survival by nitric oxide

Resistance exercise training increase activation of AKT-eNOS and Ref-1 expression by FOXO-1 activation in aorta of F344 rats

Contact Info

Product

Resources

About