Oxidized LDL Decreases
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            -Arginine Uptake and Nitric Oxide Synthase Protein Expression in Human Platelets

Chen, L.Y.; Mehta, Paulette; Mehta, Jawahar L.

doi:10.1161/01.cir.93.9.1740

Cited by 164 publications

(89 citation statements)

References 33 publications

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“…Our aim was to determine whether changes in NOS3 expression could account for the observed differences in NOS activation mediated by βAR and adenylyl cyclase. Western blotting of platelet lysates confirmed the presence of NOS3 in control and Type 2 diabetic subjects, a result consistent with previous studies [3,17,35]. No difference in basal NOS3 expression was found between platelets from control and Type 2 diabetic subjects.…”

Section: Discussionsupporting

confidence: 91%

Nitric oxide generation mediated by ?-adrenoceptors is impaired in platelets from patients with Type 2 diabetes mellitus

Queen

Goubareva

et al. 2003

Diabetologia

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Aims/hypothesis. Type 2 diabetic patients have been shown to have reduced basal platelet nitric oxide synthase activity, which is a possible contributor to the vascular complications seen in the disease. We investigated platelet nitric oxide generation stimulated by β-adrenoceptors and adenylyl cyclase in Type 2 diabetic patients and control subjects. Methods. Platelets isolated from blood taken from nine Type 2 diabetic patients and nine healthy control subjects of similar age were treated with isoproterenol 1 µmol/l, forskolin 1 µmol/l or vehicle. Platelet nitric oxide synthase activity was measured by L-[ 3 H]-arginine to L-[ 3 H]-citrulline conversion, cyclic GMP content by radioimmunoassay, and nitric oxide synthase type 3 expression by western blotting. Results. Basal platelet nitric oxide synthase activity was lower in diabetic patients than in control subjects (0.01±0.02 pmol L-citrulline/10 8 platelets, compared with 0.12±0.05; p<0.05), although no corresponding difference was seen in basal platelet cyclic GMP (0.61±0.39 and 0.13±0.22 pmol cyclic GMP/10 8 platelets respectively; p=0.37). In control subjects isoproterenol 1 µmol/l and forskolin 1 µmol/l increased platelet nitric oxide synthase activity (to 0.27±0.08 and 0.27±0.07 pmol L-citrulline/10 8 platelets respectively; p<0.05 for each in comparison with basal) and cyclic GMP (to 1.84±0.41 and 1.86±0.48; p<0.05 for each in comparison with basal). This effect was not achieved in diabetic patients. Isoproterenol-and forskolin-stimulated cyclic GMP correlated inversely with plasma glucose and HbA 1c . Platelet nitric oxide synthase type 3 expression was not different in control and diabetic subjects and was not changed by acute exposure of platelets to isoproterenol. Conclusions/interpretation. Nitric oxide generation stimulated by β-adrenoceptors and adenylyl cyclase is impaired in platelets of people with Type 2 diabetes mellitus, with no corresponding change in nitric oxide synthase type 3 expression. It is possible that this impairment contributes to the thrombotic and atherosclerotic complications of Type 2 diabetes. [Diabetologia (2003[Diabetologia ( ) 46:1474[Diabetologia ( -1482

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Section: Discussionsupporting

confidence: 91%

Nitric oxide generation mediated by ?-adrenoceptors is impaired in platelets from patients with Type 2 diabetes mellitus

Queen

Goubareva

et al. 2003

Diabetologia

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“…NO may also act as a neuroprotective or degradative agent, depending upon its concentration within the surrounding tissue [2,[14][15][16]. Aside from its aforementioned role in vasodilation, NO also plays a significant role in the modulation of platelet aggregation, smooth muscle cell proliferation, and LDL (low density lipoprotein) cholesterol oxidation within the cardiovascular system [1,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Sensors for Biological Applications

2018

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Nitric oxide (NO) is an essential signaling molecule within biological systems and is believed to be involved in numerous diseases. As a result of NO's high reaction rate, the detection of the concentration of NO, let alone the presence or absence of the molecule, is extremely difficult. Researchers have developed multiple assays and probes in an attempt to quantify NO within biological solutions, each of which has advantages and disadvantages. This review highlights many of the current NO sensors, from those that are commercially available to the newest sensors being optimized in research labs, to assist in the understanding and utilization of NO sensors in biological fields.

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“…In earlier studies, Chen et al (16) demonstrated in our laboratory that ox-LDL caused a concentration-dependent increase in thrombin-induced platelet aggregation and decreased activity. These effects were reversed by the pretreatment of platelets with L-arginine, the precursor (Fig.…”

Section: Effect On Oxidative Stressmentioning

confidence: 81%

Relevance of Platelet-independent Effects of Aspirin to Its Salutary Effect in Atherosclerosis-related Events

Khan¹,

Mehta²

2005

JAT

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There is a close inter-relationship between oxidative stress, coagulation, inflammation, and smooth muscle cell growth as key components of atherosclerosis (Fig. 1). As an analgesic and anti-pyretic, aspirin has been in use for over a century. It acetylates the COX enzyme, irreversibly inhibiting the formation of prostaglandin. Its action on platelet TxA2 has highlighted its role as an anti-thrombotic agent in cardiovascular patients. Over the last two decades, unique anti-inflammatory properties of aspirin not shared by other non-steroidals have been discovered. Aspirin biotransforms into salicylate, which has diverse but potent anti-inflammatory properties. As we strive to better understand the concepts of atherogenesis, chronic inflammation, oxidative stress, and endothelial activation, these novel effects of aspirin provide new insights as to how this wonder drug works. These effects of aspirin alter many, if not all, components of the atherogenesis cascade shown in Fig. 1

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Oxidized LDL Decreases l -Arginine Uptake and Nitric Oxide Synthase Protein Expression in Human Platelets

Abstract: These observations indicate that the L-arginine-NO pathway is involved in the effects of ox-LDL on platelet function and that ox-LDL stimulates platelet function primarily by diminishing NO synthase expression as well as decreasing the uptake of L-arginine.

Cited by 164 publications

References 33 publications

Nitric oxide generation mediated by ?-adrenoceptors is impaired in platelets from patients with Type 2 diabetes mellitus

Nitric oxide generation mediated by ?-adrenoceptors is impaired in platelets from patients with Type 2 diabetes mellitus

Nitric Oxide Sensors for Biological Applications

Relevance of Platelet-independent Effects of Aspirin to Its Salutary Effect in Atherosclerosis-related Events

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