Neurotrophins induce nitric oxide generation in human pulmonary artery endothelial cells

Meuchel, Lucas W.; Thompson, Michael A.; Cassivi, Steven D.; Pabelick, Christina M.; Prakash, Y. S.

doi:10.1093/cvr/cvr107

Cited by 65 publications

(75 citation statements)

References 59 publications

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“…BDNF and NT-3 induce relaxation of porcine pulmonary arterial rings, through activation of the endothelial nitric oxide synthase (Meuchel et al, 2011). Suppression of TrkB or TrkC expression via siRNA as well as functional blockade of p75 NTR suggest a role of both Trk and p75 NTR receptors in these effects (Meuchel et al, 2011). In our ongoing studies in rat or human pulmonary arteries, we show that NGF does not induce rat or human pulmonary arterial contraction or relaxation by itself.…”

Section: Pulmonary Hypertensionmentioning

confidence: 82%

“…A role for neurotrophins in the control of the pulmonary arterial tone was recently proposed, through activation of the p75 NTR receptor (Xu et al, 2008). BDNF and NT-3 induce relaxation of porcine pulmonary arterial rings, through activation of the endothelial nitric oxide synthase (Meuchel et al, 2011). Suppression of TrkB or TrkC expression via siRNA as well as functional blockade of p75 NTR suggest a role of both Trk and p75 NTR receptors in these effects (Meuchel et al, 2011).…”

Section: Pulmonary Hypertensionmentioning

confidence: 99%

See 1 more Smart Citation

Expression and Role of the TrkA Receptor in Pulmonary Inflammatory Diseases

Freund-Michel¹,

Müller²,

Frossard³

2011

Inflammatory Diseases - A Modern Perspective

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Section: Pulmonary Hypertensionmentioning

confidence: 82%

Section: Pulmonary Hypertensionmentioning

confidence: 99%

Expression and Role of the TrkA Receptor in Pulmonary Inflammatory Diseases

Freund-Michel¹,

Müller²,

Frossard³

2011

Inflammatory Diseases - A Modern Perspective

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“…The NO-insensitive dye 4-aminofluorescein diacetate (DAF-4) (5 M) was used as a negative control for NO detection. Cells were imaged as described previously (Meuchel et al, 2011) by using a real-time fluorescence imaging system (MetaFluor; Molecular Devices, Sunnyvale, CA) mounted on a Nikon (Tokyo, Japan) Diaphot inverted microscope, with a 40ϫ/1.3 numerical aperture oil immersion lens (Fryer Instruments, Edina, MN). Cells were initially perfused with 2.5 mM Ca 2ϩ Hanks' balanced salt solution, and baseline fluorescence was established.…”

Section: Downloaded Frommentioning

confidence: 99%

“…2A). Sensitivity of DAF-2 for NO within BECs per se was determined as described recently for pulmonary artery endothelial cells (Meuchel et al, 2011) by constructing an empirical curve of amplitudes of fluorescence changes (difference from baseline at 15 min) using a range of MAHMA-NONOate concentrations (1 nM to 10 M). Concentrations of 1 nM MAHMANONOate showed minimal changes over baseline fluorescent levels and were comparable with vehicle controls.…”

Section: Er Expression In Human Becsmentioning

confidence: 99%

Estrogen Increases Nitric-Oxide Production in Human Bronchial Epithelium

Townsend¹,

Meuchel²,

Thompson³

et al. 2011

J Pharmacol Exp Ther

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Although sex differences in asthma severity are recognized, the mechanisms by which sex steroids such as estrogen influence the airway are still under investigation. Airway tone, a key aspect of asthma, represents a balance between bronchoconstriction and dilation. Nitric oxide (NO) from the bronchial epithelium is an endogenous bronchodilator. We hypothesized that estrogens facilitate bronchodilation by generating NO in bronchial epithelium. In acutely dissociated human bronchial epithelial cells from female patients exposure to 17␤-estradiol (E 2 ; 10 pM-100 nM) resulted in rapid increase of diaminofluorescein fluorescence (NO indicator) within minutes, comparable with that induced by ATP (20 M). Estrogen receptor (ER) isoform-specific agonists (R,R)-5,11-diethyl-5,6,11,12-tetrahydro-2,8-chrysenediol (THC) (ER␣) and diaryl-propionitrile (DPN) (ER␤) stimulated NO production to comparable levels and at comparable rates, whereas the ER antagonist 7␣,17␤-[9- [(4,4,5,5,5-pentafluoropentyl)sulfinyl]nonyl]estra-1,3,5(10)-triene-3,17-diol (ICI 182,780) (1 M) was inhibitory. Estrogen effects on NO were mediated via caveolin-1 (blocked using the caveolin-1 scaffolding domain peptide) and by increased intracellular calcium concentration [prevented by 20 M 1,2-bis(oaminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid tetra(acetoxymethyl) ester but not by blocking Ca 2ϩ influx using LaCl 3 ]. Estrogen increased endothelial NO synthase activation (inhibited by 100 M N G -nitro-L-arginine methyl ester) and phosphorylated Akt. In epithelium-intact human bronchial rings contracted with acetylcholine (1 M), E 2 , THC, and DPN all produced acute bronchodilation in a dose-dependent fashion. Such bronchodilatory effects were substantially reduced by epithelial denudation. Overall, these data indicate that estrogens, acting via ER␣ or ER␤, can acutely produce NO in airway epithelium (akin to vascular endothelium). Estrogen-induced NO and its impairment may contribute to altered bronchodilation in women with asthma.

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“…In accordance with this, animal studies showed that interaction between the endothelial cells as well as cardiac contractility could not be established in the absence of BDNF in the prenatal period, followed by early postnatal death (12). Moreover, in human pulmonary artery endothelial cells BDNF substantially increased nitric oxide levels by activating Akt and endothelial nitric oxide synthase, indicating that neurotrophins acutely modulate pulmonary endothelial nitric oxide production and contribute to relaxation of the pulmonary vasculature (27).…”

Section: Bdnf Blood Level and Its Associatesmentioning

confidence: 97%

Brain derived neurotrophic factor (BDNF) in cardiometabolic physiology and diseases

Taşçı¹,

Kabul²,

Aydoğdu³

2012

Anadolu Kardiyol Derg

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Important advances in our understanding of the relationships between adipose tissue derived peptides, namely adipokines, and their effects on cardiovascular functions have been achieved in recent years. Growing knowledge of adipokine biology is revealing the complexity of these proteins. Adipose tissue releases some other proteins called neurotrophins that are mainly active in central and peripheral nervous system. However, secretion and activity of these hormones are not only limited to neuronal cells and tissues, but they also take part in adipose tissue development, energy metabolism, glucose utilization, insulin sensitivity, inflammation, lipoprotein synthesis, and atherosclerosis. In this review, we describe the most recent advances in the functions of brain derived nerve growth factor (BDNF), a major type of neurotrophins, focusing primarily on cardiovascular and metabolic diseases. (Anadolu Kardiyol Derg 2012; 12: 684-8) Key words: Brain derived nerve growth factor, cardiovascular disease, atherosclerosis, dyslipidemia, diabetes mellitus Review Derleme 684ÖZET Son yıllarda, adipokinler olarak bilinen adipoz doku kaynaklı peptidler ve bunların kardiyovasküler fonksiyonlar üzerine etkileri üzerine önemli ilerlemeler sağlanmıştır. Adipokin biyolojisi hakkında bilgiler çoğaldıkça bu proteinlerin karmaşık görünümü aydınlatılmaktadır. Adipoz doku nörotrofin-ler olarak bilinen ve temel olarak santral ve periferal sinir sisteminde görev yapan diğer bazı proteinleri de salgılar. Bununla beraber, bu hormonların sekresyon ve aktivitesi sadece nöronal hücreler ve dokularla sınırlı olmayıp yağ dokusu gelişimi, enerji metabolizması, glikoz kullanımı, insülin duyarlılığı, enflamasyon, lipoprotein sentezi ve aterosklerozda da rol oynarlar. Bu derlemede majör bir nörotrofin olan beyinden türemiş nörotrofik faktör (BDNF) ile ilgili en son veriler, özellikle kardiyovasküler ve metabolik hastalıklar üzerinden irdelenmiştir.

show abstract

Neurotrophins induce nitric oxide generation in human pulmonary artery endothelial cells

Abstract: These results indicate that NTs acutely modulate pulmonary endothelial NO production and contribute to relaxation of the pulmonary vasculature.

Cited by 65 publications

References 59 publications

Expression and Role of the TrkA Receptor in Pulmonary Inflammatory Diseases

Expression and Role of the TrkA Receptor in Pulmonary Inflammatory Diseases

Estrogen Increases Nitric-Oxide Production in Human Bronchial Epithelium

Brain derived neurotrophic factor (BDNF) in cardiometabolic physiology and diseases

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