Endothelial Nitric-oxide Synthase Activation Generates an Inducible Nitric-oxide Synthase-like Output of Nitric Oxide in Inflamed Endothelium

Lowry, Jessica; Brovkovych, Viktor; Zhang, Yongkang; Skidgel, Randal A.

doi:10.1074/jbc.m112.436022

Cited by 47 publications

(38 citation statements)

References 90 publications

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“…Therefore, we investigated the possibility that ERK and JNK activation also contribute to LPS-induced STIM1 expression in HLMVECs. Here we used a pharmacological approach to prevent the activation of ERK and JNK in HLMVECs (42). We observed that the ERK inhibitor PD98059 prevented LPS-induced ERK phosphorylation (Fig.…”

Section: Lps Priming In Vivo Potentiates Par-1-induced Increase In Lumentioning

confidence: 99%

Cooperative Signaling via Transcription Factors NF-κB and AP1/c-Fos Mediates Endothelial Cell STIM1 Expression and Hyperpermeability in Response to Endotoxin

DebRoy

Vogel

Soni

et al. 2014

Journal of Biological Chemistry

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Background: STIM1 activates store-operated Ca 2ϩ entry (SOCE). The transcriptional regulation of STIM1 during sepsis is not known. Results: STIM1 expression occurs downstream of TLR4 via activation of NF-B and p38␣-mediated c-Fos expression in endothelial cells. Conclusion: Cooperative signaling of NF-B and p38 MAPK downstream of TLR4 is essential for STIM1 expression during sepsis. Significance: Selective p38␣ inhibitors may represent a potential therapeutic strategy to prevent sepsis-mediated lung vascular leaks.

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Section: Lps Priming In Vivo Potentiates Par-1-induced Increase In Lumentioning

confidence: 99%

Cooperative Signaling via Transcription Factors NF-κB and AP1/c-Fos Mediates Endothelial Cell STIM1 Expression and Hyperpermeability in Response to Endotoxin

DebRoy

Vogel

Soni

et al. 2014

Journal of Biological Chemistry

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“…As a result of experiments conducted in the presence of frovatriptan (5×10 -5 mol/l), the contractile response to L-norepinephrine was signifi cantly increased compared to control reaction on the carotid artery. Our results also suggest that frovatriptan predominantly at higher concentrations probably by non-specifi c mechanism, which could activate the following intracellular chain reaction: stimulation on α 1D → activation of eNOS → increase in the concentration of NO 16 and subsequent relaxation, which is atypical for the triptans.…”

Section: Effects Of 5×10 -5 Mol/l Frovatriptan On the Con-tractile Acmentioning

confidence: 76%

Effects of the Novel High-affinity 5-HT(1B/1D)-receptor Ligand Frovatriptan on the Rat Carotid Artery

et al. 2017

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Citation: Saracheva KE, Prissadova NA, Turiiski VI, Slavchev VI, Krastev AD, Getova DP. Effects of the novel high-affi nity 5-HT(1B/1D)-receptor ligand frovatriptan on the rat carotid artery.Folia Medica 2017;59(1): 31-36. doi: 10.1515/folmed-2017-0006 Background: In blood vessels 5-HT stimulates sympathetic nerves, the endothelium and vascular smooth muscle cells. Triptans are specifi c anti-migraine drugs and they activate the serotoninergic 5HT1b/d receptors causing vasoconstriction of the cerebral vessels. Aim: To evaluate the eff ect of frovatriptan on isolated rat carotid artery. Methods: Contractile activity of the preparations was registered isometrically. Krebs solution (pH = 7.4) was used for washing smooth muscle (SM) preparations aerated with 95% O 2 and 5% CO 2 at 37°C. The 60-minute adaptation of tone level of preparations was taken as a starting tone and the changes such as contraction or relaxation were calculated using it. Results: Frovatriptan (1×10 -6 mol/l -1×10 -5 mol/l) induced a contraction, but at higher concentrations it caused relaxation of the carotid artery. The L-norepinephrine contractile reaction was enhanced in the presence of frovatriptan. In the presence of 5-HT2 receptor antagonist, methysergide, frovatriptan increased the relaxation. In the presence of the specifi c α-1 receptor antagonist, prazosin, the frovatriptan-induced relaxation decreased. Conclusion:The observed contractile eff ect of frovatriptan is probably associated with the main eff ect of the drug -activation of the serotoninergic 5HT 1B /1D receptors causing vasoconstriction of the cerebral vessels and their anti-migraine eff ect. At higher concentrations, frovatriptan, most likely via some non-specifi c mechanism, could activate the following intracellular chain reaction: stimulation of α 1D could activate eNOS which may increase in the concentration of NO which results in the fi nal eff ect of relaxation. BACKGROUND

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“…NO causes a decrease in platelet cytosolic Ca 2+ , which influences platelet glycoprotein activation, and therefore, platelet adhesion (63). NO can also inhibit fibrin deposition, further attenuating thrombus formation (137). In contrast, EC-generated ROS acts to promote platelet activation and aggregation (42 Figure 3 The role of the pulmonary endothelium in platelet function.…”

Section: Coagulationmentioning

confidence: 98%

Endothelial Cell Regulation of Pulmonary Vascular Tone, Inflammation, and Coagulation

Goldenberg

Kuebler

2015

Comprehensive Physiology

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The pulmonary endothelium represents a heterogeneous cell monolayer covering the luminal surface of the entire lung vasculature. As such, this cell layer lies at a critical interface between the blood, airways, and lung parenchyma, and must act as a selective barrier between these diverse compartments. Lung endothelial cells are able to produce and secrete mediators, display surface receptor, and cellular adhesion molecules, and metabolize circulating hormones to influence vasomotor tone, both local and systemic inflammation, and coagulation functions. In this review, we will explore the role of the pulmonary endothelium in each of these systems, highlighting key regulatory functions of the pulmonary endothelial cell, as well as novel aspects of the pulmonary endothelium in contrast to the systemic cell type. The interactions between pulmonary endothelial cells and both leukocytes and platelets will be discussed in detail, and wherever possible, elements of endothelial control over physiological and pathophysiological processes will be examined. C 2015 American Physiological Society.

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Endothelial Nitric-oxide Synthase Activation Generates an Inducible Nitric-oxide Synthase-like Output of Nitric Oxide in Inflamed Endothelium

Cited by 47 publications

References 90 publications

Cooperative Signaling via Transcription Factors NF-κB and AP1/c-Fos Mediates Endothelial Cell STIM1 Expression and Hyperpermeability in Response to Endotoxin

Cooperative Signaling via Transcription Factors NF-κB and AP1/c-Fos Mediates Endothelial Cell STIM1 Expression and Hyperpermeability in Response to Endotoxin

Effects of the Novel High-affinity 5-HT(1B/1D)-receptor Ligand Frovatriptan on the Rat Carotid Artery

Endothelial Cell Regulation of Pulmonary Vascular Tone, Inflammation, and Coagulation

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