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Pulmonary endothelium

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https://www.readbyqxmd.com/read/27919660/a-comparison-of-vasodilation-mode-among-selexipag-ns-304-2-4-5-6-diphenylpyrazin-2-yl-isopropyl-amino-butoxy-n-methylsulfonyl-acetamide-its-active-metabolite-mre-269-and-various-prostacyclin-receptor-agonists-in-rat-porcine-and-human-pulmonary-arteries
#1
Chiaki Fuchikami, Kohji Murakami, Koyuki Tajima, Junko Homan, Keiji Kosugi, Kazuya Kuramoto, Michiko Oka, Keiichi Kuwano
Selexipag (NS-304; [2-{4-[(5,6-diphenylpyrazin-2-yl)(isopropyl)amino]butoxy}-N- (methylsulfonyl)acetamide]) is a novel, orally available non-prostanoid prostacyclin receptor (IP receptor) agonist that has recently been approved for the treatment of pulmonary arterial hypertension (PAH). We examined the effect of the active metabolite of selexipag, MRE-269, and IP receptor agonists that are currently available as PAH therapeutic drugs on the relaxation of rat, porcine and human pulmonary artery. cAMP formation in human pulmonary artery smooth muscle cells was induced by all test compounds (MRE-269, epoprostenol, iloprost, treprostinil and beraprost sodium) and suppressed by IP receptor antagonists (CAY10441 and 2-[4-(1H-indol-4-yloxymethyl)-benzyloxycarbonylamino]-3-phenyl-propionic acid)...
December 2, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27884766/mechanisms-of-vascular-dysfunction-in-copd-and-effects-of-a-novel-soluble-epoxide-hydrolase-inhibitor-in-smokers
#2
Lucy Yang, Joseph Cheriyan, David D Gutterman, Ruth J Mayer, Zsuzsanna Ament, Jules L Griffin, Aili L Lazaar, David E Newby, Ruth Tal-Singer, Ian B Wilkinson
BACKGROUND: Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for cardiovascular disease, and the pathogenesis may involve endothelial dysfunction. We tested the hypothesis that endothelium-derived epoxyeicosatrienoic acid (EET)-mediated endothelial function is impaired in patients with COPD, and a novel sEH inhibitor GSK2256294 attenuates EET-mediated endothelial dysfunction in human resistance vessels both in vitro and in vivo. METHODS: Endogenous and stimulated endothelial release of EETs was assessed in 12 COPD patients, 11 overweight smokers, and 2 matched control groups, using forearm plethysmography with intra-arterial infusions of fluconazole, bradykinin, and the combination...
November 21, 2016: Chest
https://www.readbyqxmd.com/read/27871277/pulmonary-endothelial-activation-caused-by-extracellular-histones-contributes-to-neutrophil-activation-in-acute-respiratory-distress-syndrome
#3
Yanlin Zhang, Li Guan, Jie Yu, Zanmei Zhao, Lijun Mao, Shuqiang Li, Jinyuan Zhao
BACKGROUND: During the acute respiratory distress syndrome (ARDS), neutrophils play a central role in the pathogenesis, and their activation requires interaction with the endothelium. Extracellular histones have been recognized as pivotal inflammatory mediators. This study was to investigate the role of pulmonary endothelial activation during the extracellular histone-induced inflammatory response in ARDS. METHODS: ARDS was induced in male C57BL/6 mice by intravenous injection with lipopolysaccharide (LPS) or exogenous histones...
November 21, 2016: Respiratory Research
https://www.readbyqxmd.com/read/27865192/effect-of-targeted-therapy-on-circulating-progenitor-cells-in-precapillary-pulmonary-hypertension
#4
Jéssica García-Lucio, Olga Tura-Ceide, Roberto Del Pozo, Isabel Blanco, Sandra Pizarro, Elisabet Ferrer, Marta Díez, Núria Coll-Bonfill, Lucilla Piccari, Víctor I Peinado, Joan Albert Barberà
BACKGROUND: Endothelial dysfunction is key in the development of pulmonary hypertension (PH) and is associated with reduced number of circulating progenitor cells. Studies to date evaluating levels of circulating progenitor cells in PH have provided conflicting results. Current treatment of pulmonary arterial hypertension (PAH) and medical treatment of chronic thromboembolic pulmonary hypertension (CTEPH) targets endothelium dependent signalling pathways. The effect of PAH-targeted therapy on circulating progenitor cells has not been clearly established...
November 9, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/27858190/nitro-oleic-acid-prevents-hypoxia-and-asymmetric-dimethylarginine-induced-pulmonary-endothelial-dysfunction
#5
Adolf Koudelka, Gabriela Ambrozova, Anna Klinke, Tana Fidlerova, Hana Martiskova, Radek Kuchta, Tanja K Rudolph, Jaroslav Kadlec, Zdenka Kuchtova, Steven R Woodcock, Bruce A Freeman, Lukas Kubala, Michaela Pekarova
RATIONALE: Pulmonary hypertension (PH) represents a serious health complication accompanied with hypoxic conditions, elevated levels of asymmetric dimethylarginine (ADMA), and overall dysfunction of pulmonary vascular endothelium. Since the prevention strategies for treatment of PH remain largely unknown, our study aimed to explore the effect of nitro-oleic acid (OA-NO2), an exemplary nitro-fatty acid (NO2-FA), in human pulmonary artery endothelial cells (HPAEC) under the influence of hypoxia or ADMA...
November 17, 2016: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/27855271/experimental-lung-injury-reduces-klf2-to-increase-endothelial-permeability-via-regulation-of-rapgef3-rac1-signaling
#6
Ru-Ting Huang, David Wu, Angelo Meliton, Myung-Jin Oh, Matthew Krause, Joyce A Lloyd, Recep Nigdelioglu, Robert B Hamanaka, Mukesh K Jain, Anna Birukova, John P Kress, Konstantin G Birukov, Gökhan M Mutlu, Yun Fang
RATIONALE: The acute respiratory distress syndrome (ARDS) is caused by widespread endothelial barrier disruption and uncontrolled cytokine storm. Genome-wide association studies (GWAS) have linked multiple genes to ARDS. Although mechano-sensitive transcription factor Krüppel-like factor 2 (KLF2) is a major regulator of endothelial function, its role in regulating pulmonary vascular integrity in lung injury and ARDS-associated GWAS genes remains poorly understood. OBJECTIVES: To examine KLF2 expression in multiple animal models of acute lung injury and further elucidate the KLF2-mediated pathways involved in endothelial barrier disruption and cytokine storm in experimental lung injury...
November 17, 2016: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/27798647/gene-expression-profiling-of-pulmonary-artery-in-a-rabbit-model-of-pulmonary-thromboembolism
#7
Zhiyuan Tang, Xudong Wang, Jianfei Huang, Xiaoyu Zhou, Hao Xie, Qilin Zhu, Minjie Huang, Songshi Ni
Acute pulmonary thromboembolism (PTE) refers to the obstruction of thrombus in pulmonary artery or its branches. Recent studies have suggested that PTE-induced endothelium injury is the major physiological consequence of PTE. And it is reasonal to use PTE-induced endothelium injury to stratify disease severity. According to the massive morphologic and histologic findings, rabbit models could be applied to closely mimic the human PE. Genomewide gene expression profiling has not been attempted in PTE. In this study, we determined the accuracy of rabbit autologous thrombus PTE model for human PTE disease, then we applied gene expression array to identify gene expression changes in pulmonary arteries under PTE to identify potential molecular biomarkers and signaling pathways for PTE...
2016: PloS One
https://www.readbyqxmd.com/read/27795403/the-andes-virus-nucleocapsid-protein-directs-basal-endothelial-cell-permeability-by-activating-rhoa
#8
Elena E Gorbunova, Matthew J Simons, Irina N Gavrilovskaya, Erich R Mackow
: Andes virus (ANDV) predominantly infects microvascular endothelial cells (MECs) and nonlytically causes an acute pulmonary edema termed hantavirus pulmonary syndrome (HPS). In HPS patients, virtually every pulmonary MEC is infected, MECs are enlarged, and infection results in vascular leakage and highly lethal pulmonary edema. We observed that MECs infected with the ANDV hantavirus or expressing the ANDV nucleocapsid (N) protein showed increased size and permeability by activating the Rheb and RhoA GTPases...
October 25, 2016: MBio
https://www.readbyqxmd.com/read/27792124/erythrocyte-derived-microparticles-activate-pulmonary-endothelial-cells-in-a-murine-model-of-transfusion
#9
Alex L Chang, Young Kim, Aaron P Seitz, Rebecca M Schuster, Alex B Lentsch, Timothy A Pritts
Erythrocyte-derived microparticles (MPs) are sub-micrometer, biologically active vesicles shed by red blood cells as part of the biochemical changes that occur during storage. We hypothesized that MPs from stored red blood cells would activate endothelial cells. MPs from aged murine packed red blood cells (pRBCs) were isolated and used to treat confluent layers of cultured endothelial cells. Endothelial expression of leukocyte adhesion molecules, ELAM-1 and ICAM-1, and inflammatory mediator, IL-6, were evaluated at 0...
October 27, 2016: Shock
https://www.readbyqxmd.com/read/27765042/circulating-microparticles-in-severe-pulmonary-arterial-hypertension-increase-intercellular-adhesion-molecule-1-expression-selectively-in-pulmonary-artery-endothelium
#10
Leslie A Blair, April K Haven, Natalie N Bauer
BACKGROUND: Microparticles (MPs) stimulate inflammatory adhesion molecule expression in systemic vascular diseases, however it is unknown whether circulating MPs stimulate localized ICAM-1 expression in the heterogeneically distinct pulmonary endothelium during pulmonary arterial hypertension (PAH). Pulmonary vascular lesions with infiltrating inflammatory cells in PAH form in the pulmonary arteries and arterioles, but not the microcirculation. Therefore, we sought to determine whether circulating MPs from PAH stimulate pulmonary artery endothelial cell-selective ICAM-1 expression...
October 20, 2016: Respiratory Research
https://www.readbyqxmd.com/read/27754034/yia-03-10-endothelial-kruppel-like-factor-15-a-novel-target-for-the-treatment-of-pulmonary-hypertension
#11
Deepesh Pandey, Daijiro Tori, Yohei Nomura, Dan Berkowitz, Lewis Romer
OBJECTIVE: Kruppel Like Factor 15 (KLF15) has recently been shown to be critical for activation of proinflammatory processes in vascular smooth muscle and atherogenesis. Although KLF15 is abundantly expressed in vascular endothelium there is a significant lack of knowledge regarding the role of KLF15 in the regulation of vascular endothelial function. Here we tested the hypothesis that KLF15 is a critical regulator of Arg2 transcription in hypoxia exposed human pulmonary microvascular endothelial cells (HPMEC) and that it plays critical role in pathogenesis of pulmonary hypertension (PHTN)...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27746862/hyperbaric-environment-up-regulates-cd15s-expression-on-leukocytes-down-regulates-cd77-expression-on-renal-cells-and-up-regulates-cd34-expression-on-pulmonary-and-cardiac-cells-in-rat
#12
Danka Đevenica, Anita Markotić, Nikolina Režić-Mužinić, Igor Jelaska, Tatijana Zemunik, Hrvoje Delić, Vedrana Čikeš Čulić
OBJECTIVES: The aim of this study was to estimate effects of hyperbaric (HB) treatment by determination of CD15s and CD11b leukocyte proinflammatory markers expression. In addition, this study describes changes in CD77 and CD34 expression on rat endothelial cells in renal, pulmonary and cardiac tissue following exposure to hyperbaric pressure. MATERIALS AND METHODS: Expression of CD11b and CD15s on leukocytes, as well as CD77 and CD34 expression on endothelial cells in cell suspensions of renal, pulmonary and cardiac tissue in rats after hyperbaric treatment and in control rats were determined by flow cytometry...
August 2016: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/27723048/epizootic-haemorrhagic-disease-virus-induced-apoptosis-in-bovine-carotid-artery-endothelium-is-p53-independent
#13
Prachi Sharma, David E Stallknecht, Elizabeth W Howerth
Epizootic haemorrhagic disease virus (EHDV) replicates in endothelium and it has been shown that EHDV serotype 2 (Ibaraki) is able to cause cell death by apoptosis in cow pulmonary artery endothelial cells. However, the underlying mechanism has not been established. For some viruses, such as influenza, a p53 dependent mechanism has been demonstrated in viral induced apoptosis. In this study, we investigate the involvement of p53 in the induction of apoptosis in a US isolate of EHDV serotype 2 in cow endothelium...
September 30, 2016: Veterinaria Italiana
https://www.readbyqxmd.com/read/27720762/pharmacological-analysis-of-hemodynamic-responses-to-lachesis-muta-south-american-bushmaster-snake-venom-in-anesthetized-rats
#14
Lourdes Dias, Mariana A P Rodrigues, Bruna R Inoue, Renata L Rodrigues, André L Rennó, Valéria B de Souza, Frank D Torres-Huaco, Norma C Sousa, Alessandra Stroka, Anibal R Melgarejo, Stephen Hyslop
In this work, we examined some mechanisms involved in the hypotension caused by Lachesis muta (South American bushmaster) venom in anesthetized rats. Venom (1.5 mg/kg, i.v.) caused immediate hypotension that was maximal after 5 min and gradually returned to baseline over 60 min. Pretreatment of rats with the non-selective nitric oxide synthase (NOS) inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME) did not attenuate the early phase of venom-induced hypotension, but abolished the recovery phase and resulted in rapid death; a similar effect was observed with the soluble guanylate cyclase (sGC) inhibitor ODQ...
October 5, 2016: Toxicon: Official Journal of the International Society on Toxinology
https://www.readbyqxmd.com/read/27707929/constitutively-expressed-ifitm3-protein-in-human-endothelial-cells-poses-an-early-infection-block-to-human-influenza-viruses
#15
Xiangjie Sun, Hui Zeng, Amrita Kumar, Jessica A Belser, Taronna R Maines, Terrence M Tumpey
: A role for pulmonary endothelial cells in the orchestration of cytokine production and leukocyte recruitment during influenza virus infection, leading to severe lung damage, has been recently identified. As the mechanistic pathway for this ability is not fully known, we extended previous studies on influenza virus tropism in cultured human pulmonary endothelial cells. We found that a subset of avian influenza viruses, including potentially pandemic H5N1, H7N9, and H9N2 viruses, could infect human pulmonary endothelial cells (HULEC) with high efficiency compared to human H1N1 or H3N2 viruses...
December 15, 2016: Journal of Virology
https://www.readbyqxmd.com/read/27669126/endothelial-cell-senescence-and-thrombosis-ageing-clots
#16
REVIEW
Magdalena L Bochenek, Eva Schütz, Katrin Schäfer
Age is an important cardiovascular risk factor. Among others, age is associated with an increased risk to develop thrombotic cardiovascular complications, both in the arterial (acute myocardial infarction, stroke) and the venous (deep vein thrombosis, pulmonary embolism) system, which cannot be explained by the age-associated increase in cardiovascular risk factors alone. A number of studies have demonstrated that the accumulation of senescent endothelial cells and specific phenotypic and functional alterations associated with endothelial cell senescence may play an important role during the development and progression of cardiovascular disease...
November 2016: Thrombosis Research
https://www.readbyqxmd.com/read/27667662/antibodies-to-major-histocompatibility-complex-class-ii-antigens-directly-prime-neutrophils-and-cause-acute-lung-injury-in-a-two-event-in-vivo-rat-model
#17
Marguerite R Kelher, Anirban Banerjee, Fabia Gamboni, Cameron Anderson, Christopher C Silliman
BACKGROUND: Transfusion-related acute lung injury (TRALI) is a significant cause of mortality, especially after transfusions containing antibodies to major histocompatibility complex (MHC) class II antigens. We hypothesize that a first event induces both 1) polymorphonuclear neutrophils (PMNs) to express MHC class II antigens, and 2) activation of the pulmonary endothelium, leading to PMN sequestration, so that the infusion of specific MHC class II antibodies to these antigens causes PMN-mediated acute lung injury (ALI)...
December 2016: Transfusion
https://www.readbyqxmd.com/read/27664754/the-ep1-ep3-receptor-agonist-17-pt-pge2-acts-as-an-ep4-receptor-agonist-on-endothelial-barrier-function-and-in-a-model-of-lps-induced-pulmonary-inflammation
#18
Theiler Anna, Konya Viktoria, Pasterk Lisa, Maric Jovana, Bärnthaler Thomas, Lanz Ilse, Platzer Wolfgang, Schuligoi Rufina, Heinemann Akos
Endothelial dysfunction is a hallmark of inflammatory conditions. We recently demonstrated that prostaglandin (PG)E2 enhances the resistance of pulmonary endothelium in vitro and counteracts lipopolysaccharide (LPS)-induced pulmonary inflammation in vivo via EP4 receptors. The aim of this study was to investigate the role of the EP1/EP3 receptor agonist 17-phenyl-trinor-(pt)-PGE2 on acute lung inflammation in a mouse model. In LPS-induced pulmonary inflammation in mice, 17-pt.-PGE2 reduced neutrophil infiltration and inhibited vascular leakage...
September 21, 2016: Vascular Pharmacology
https://www.readbyqxmd.com/read/27663990/regulation-of-pulmonary-endothelial-barrier-function-by-kinases
#19
REVIEW
Nektarios Barabutis, Alexander Verin, John D Catravas
The pulmonary endothelium is the target of continuous physiological and pathological stimuli that affect its crucial barrier function. The regulation, defense, and repair of endothelial barrier function require complex biochemical processes. This review examines the role of endothelial phosphorylating enzymes, kinases, a class with profound, interdigitating influences on endothelial permeability and lung function.
November 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/27650575/selective-targeting-of-il-2-to-nkg2d-bearing-cells-for-improved-immunotherapy
#20
Reza Ghasemi, Eric Lazear, Xiaoli Wang, Saeed Arefanian, Alexander Zheleznyak, Beatriz M Carreno, Ryuji Higashikubo, Andrew E Gelman, Daniel Kreisel, Daved H Fremont, Alexander Sasha Krupnick
Despite over 20 years of clinical use, IL-2 has not fulfilled expectations as a safe and effective form of tumour immunotherapy. Expression of the high affinity IL-2Rα chain on regulatory T cells mitigates the anti-tumour immune response and its expression on vascular endothelium is responsible for life threatening complications such as diffuse capillary leak and pulmonary oedema. Here we describe the development of a recombinant fusion protein comprised of a cowpox virus encoded NKG2D binding protein (OMCP) and a mutated form of IL-2 with poor affinity for IL-2Rα...
September 21, 2016: Nature Communications
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