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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/30399322/bitter-taste-receptors-taking-a-bigger-bite-of-airway-smooth-muscle-pathophysiology
#1
Charles W Emala
No abstract text is available yet for this article.
November 6, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30395484/direct-inhibitory-effect-of-the-phosphodiesterase-4-inhibitor-roflumilast-on-neutrophil-migration-in-copd
#2
Amy E Dunne, Theerasuk Kawamatawong, Peter S Fenwick, Ceri M Davies, Hannah Tullett, Peter J Barnes, Louise E Donnelly
Neutrophilic inflammation is characteristic of COPD, yet there are no effective anti-inflammatory therapies. The phosphodiesterase (PDE)4 inhibitor, roflumilast is approved for use in COPD and suppresses sputum neutrophilia. The mechanism underlying this observation is unclear and therefore this study addressed whether roflumilast directly affected neutrophil migration. Blood-derived neutrophils were isolated from non-smokers, smokers and COPD patients and chemotaxis measured using Boyden chambers. Intracellular calcium ion concentration ([Ca2+]i) was measured by fluorimetry and shape change and CD11b expression by flow cytometry...
November 5, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30383397/there-is-no-smoke-without-mitochondria
#3
SeungHye Han, Navdeep S Chandel
No abstract text is available yet for this article.
November 1, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30383396/autophagy-activation-in-asthma-airways-remodeling
#4
Kielan D McAlinden, Deepak A Deshpande, Saeid Ghavami, Dia Xenaki, Sukhwinder Singh Sohal, Brian G Oliver, Mehra Haghi, Pawan Sharma
Current asthma therapies fail to target airway remodeling which correlates with asthma severity driving disease progression that ultimately leads to loss of lung function. Macroautophagy (here after autophagy) is a fundamental cell recycling mechanism in all eukaryotic cells; emerging evidence suggests that it is dysregulated in asthma. We investigated the interrelationship between autophagy and airway remodeling and assessed preclinical efficacy of a known autophagy inhibitor in murine models of asthma. Human asthmatic and non-asthmatic lung tissues were histologically evaluated and were immuno-stained for key autophagy markers...
November 1, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30376354/identifying-copd-genes-shining-the-light-on-dark-dna
#5
Josiah E Radder, Steven D Shapiro
No abstract text is available yet for this article.
October 30, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30376353/emapii-a-key-player-in-hiv-nef-induced-pulmonary-vasculopathy
#6
Elya A Shamskhou, Leah Verghese, Ke Yuan, Vinicio A De Jesus Perez
No abstract text is available yet for this article.
October 30, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30372120/how-the-respiratory-epithelium-senses-and-reacts-to-influenza-virus
#7
Kambez H Benam, Laura Denney, Ling-Pei Ho
Our lungs are constantly exposed to the environment and potential pathogens. As the interface between host and environment, the respiratory epithelium has evolved sophisticated sensing mechanisms as part of its defence against pathogens. In this review, we examine how the respiratory epithelium senses and responds to influenza A virus (IAV), the biggest cause of respiratory viral deaths worldwide.
October 29, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30372117/outsourcing-invasion-a-novel-function-for-extracellular-vesicles-in-the-lung
#8
Tzu-Pin Shentu, James S Hagood
No abstract text is available yet for this article.
October 29, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30365353/tanking-influenza-a-virus-in-the-lung
#9
Sarah Rosli, Michelle D Tate
No abstract text is available yet for this article.
October 26, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30365342/aiming-immunomodulation-therapy-at-sepsis
#10
Aleksandra Leligdowicz, Michael A Matthay
No abstract text is available yet for this article.
October 26, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30365340/biased-tas2r-bronchodilators-inhibit-airway-smooth-muscle-growth-by-downregulating-perk1-2
#11
Donghwa Kim, Soomin Cho, Maria A Castaño, Reynold A Panettieri, Jung A Woo, Stephen B Liggett
Bitter taste receptor (TAS2R) agonists dilate airways by receptor-dependent smooth muscle relaxation. Besides coupling to relaxation, we have found that human airway smooth muscle (HASM) cell TAS2Rs activate (phosphorylate) ERK1/2, but the cellular effects are not known. Here we show in HASM cells that TAS2R agonists initially stimulate pERK1/2, but by 24 hrs cause a marked (50-70%) downregulation of pERK1/2 without a change in total ERK1/2. It was hypothesized that TAS2R agonists suppress cell growth through this pERK1/2 downregulation...
October 26, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30359079/integrins-%C3%AE-v%C3%AE-5-and-%C3%AE-v%C3%AE-6-mediate-il-4-induced-collective-migration-in-human-airway-epithelial-cells
#12
Sang-Nam Lee, Ji-Suk Ahn, Seong Gyu Lee, Jin-Ah Park, Hyung-Suk Lee, Augustine M K Choi, Joo-Heon Yoon
A positive link between persistent cellular motion and a defective tight junction (TJ) barrier allows increased antigenic penetration and contact between ligand/receptor pairs, leading to exacerbated allergic airway inflammation and remodeling. Given that collective cell migration involves cell-cell and cell-extracellular matrix (ECM) adhesions, and that interleukin-4 (IL-4) induces epithelial barrier dysfunction and decreases cell-ECM adhesions, we hypothesized that IL-4 may induce collective migration in the well-differentiated primary human nasal epithelial cells (HNECs)...
October 25, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30359078/contractile-properties-of-intrapulmonary-airway-smooth-muscle-in-cystic-fibrosis
#13
Oleg S Matusovsky, Linda Kachmar, Gijs Ijpma, Alice Panariti, Andrea Benedetti, James G Martin, Anne-Marie Lauzon
RATIONALE: Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane conductance regulator gene. Many CF patients have asthma-like symptoms and airway hyperresponsiveness (AHR) which are potentially associated with altered airway smooth muscle (ASM) contractility. The goal of this study was to assess the contractility of the CF intrapulmonary ASM. METHODS: ASM strips were dissected from human control and CF intrapulmonary airways and assessed for methacholine (MCh)-induced shortening velocity, maximal force and stress...
October 25, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30352167/leukotriene-a4-hydrolase-activation-and-leukotriene-b4-production-by-eosinophils-in-severe-asthma
#14
Kavita Pal, Xin Feng, John W Steinke, Marie D Burdick, Yun M Shim, Sun-Sang Sung, W Gerald Teague, Larry Borish
RATIONALE: Asthma is associated with the over-production of leukotrienes (LT) including LTB4. Severe asthma patients can be highly responsive to 5-LO inhibition, which blocks production of both the cysteinyl LTs and LTB4. Production of LTB4 has traditionally been ascribed to neutrophils, mononuclear phagocytes and epithelial cells and acts as a chemoattractant for inflammatory cells associated with asthma. The source of LTB4 is unclear, especially in eosinophilic asthma. We speculated that the benefit of 5-LO inhibition could be mediated, in part, by inhibition of eosinophil-derived LTB4...
October 23, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30339463/marcks-myristoylated-alanine-rich-c-kinase-substrate-and-lung-disease
#15
Mary K Sheats, Qi Yin, Shijing Fang, Joungjoa Park, Anne L Crews, Indu Parikh, Brian Dickson, Kenneth B Adler
MARCKS (Myristoylated Alanine Rich C Kinase Substrate) is a prominent Protein Kinase C (PKC) substrate expressed in all eukaryotic cells. It is known to bind to and cross-link actin filaments, to serve as a bridge between Ca++/Calmodulin (CaM) and PKC signaling, and to sequester the signaling molecule phosphatidylinositol 4,5-bisphosphate PI(4,5)P2 (PIP2) in the plasma membrane (1-6). Since the mid 1980's, this evolutionarily - conserved and ubiquitously - expressed protein has been associated with regulating cellular events that require dynamic actin reorganization, including cellular adhesion, migration and exocytosis (7-21)...
October 19, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30339461/alternative-oxidase-attenuates-cigarette-smoke-induced-lung-dysfunction-and-tissue-damage
#16
Luca Giordano, Antoine Farnham, Praveen K Dhandapani, Laura Salminen, Jahnavi Bhaskaran, Robert Voswinckel, Peter Rauschkolb, Susan Scheibe, Natascha Sommer, Christoph Beisswenger, Norbert Weissmann, Thomas Braun, Howard T Jacobs, Robert Bals, Christian Herr, Marten Szibor
Cigarette-smoke (CS) exposure is the predominant risk factor for the development of chronic obstructive pulmonary disease (COPD) and the third leading cause of death worldwide. We aimed to elucidate if mitochondrial respiratory inhibition and oxidative stress are triggers in its etiology. In different models of CS exposure, we investigated the effect on lung remodeling and cell signaling of restoring mitochondrial respiratory electron flow, using the alternative oxidase (AOX), which by-passes the cytochrome segment of the respiratory chain...
October 19, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30335513/lessons-from-transcriptomics-in-hypoxia-induced-pulmonary-hypertension-does-the-mouse-strain-matter
#17
Leigh M Marsh, Grazyna Kwapiszewska
No abstract text is available yet for this article.
October 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30335480/integrative-genomics-analysis-identifies-acvr1b-as-a-candidate-causal-gene-of-emphysema-distribution
#18
Adel Boueiz, Betty Pham, Robert Chase, Andrew Lamb, Sool Lee, Zun Zar Chi Naing, Michael H Cho, Margaret M Parker, Phuwanat Sakornsakolpat, Craig P Hersh, James D Crapo, Andrew B Stergachis, Ruth Tal-Singer, Dawn L DeMeo, Edwin K Silverman, Xiaobo Zhou, Peter J Castaldi
RATIONALE: Genome-wide association studies (GWAS) have identified multiple associations with emphysema apico-basal distribution (EABD), but the biological functions of these variants are unknown. METHODS: To characterize the functions of EABD-associated variants, we integrated GWAS results with 1) expression quantitative trait loci (eQTL) from the GTEx project and subjects in the COPDGene Study and 2) cell type epigenomic marks from the Roadmap Epigenomics project...
October 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30335467/secretory-inositol-polyphosphate-4-phosphatase-protects-against-airway-inflammation-and-remodeling
#19
Kritika Khanna, Rituparna Chaudhuri, Jyotirmoi Aich, Bijay Pattnaik, Lipsa Panda, Y S Prakash, Ulaganathan Mabalirajan, Balaram Ghosh, Anurag Agrawal
The asthma candidate gene, inositol polyphosphate 4-phosphatase (INPP4A) is a lipid phosphatase that negatively regulates the phosphoinositide-3-kinase (PI3K)/Akt pathway. Destabilizing genetic variants of INPP4A increase asthma risk and lung-specific INPP4A knockdown induces asthma-like features. INPP4A is known to localise intracellularly and its extracellular presence has not been reported yet. Here we show for the first time that INPP4A is secreted by airway epithelial cells and that extracellular INPP4A critically inhibits airway inflammation and remodeling...
October 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/30326743/therapeutic-targeting-of-apoptosis-inhibitor-of-macrophage-aim-cd5l-in-sepsis
#20
Xun Gao, Xingxing Yan, Yibing Yin, Xue Lin, Qun Zhang, Yun Xia, Ju Cao
The factors involved in disturbing host homeostasis during sepsis are largely unknown. We sought to determine the immunopathlogical role of apoptosis inhibitor of macrophage (AIM)/CD5L in sepsis. Here we showed that blockade of AIM led to significantly increased survival after experimental sepsis, and it decreased local and systemic inflammation, reduced tissue injury, and inhibited bacterial dissemination in the blood in particular at later time points. Supplementation of recombinant AIM in sepsis resulted in increased tissue injury, amplified inflammation, increased bacteremia, and worsened mortality...
October 16, 2018: American Journal of Respiratory Cell and Molecular Biology
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