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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/28812922/a-circulating-micro-rna-signature-serves-as-a-diagnostic-and-prognostic-indicator-in-sarcoidosis
#1
Christian Ascoli, Yue Huang, Cody Schott, Benjamin A Turturice, Ahmed Metwally, David L Perkins, Patricia W Finn
Micro-RNAs (miRNAs) act as post-transcriptional regulators of gene expression. In sarcoidosis, aberrant miRNA expression may enhance immune responses mounted against an unknown antigenic agent. We tested whether a distinct miRNA signature functions as a diagnostic biomarker and explored its role as an immune modulator in sarcoidosis. Expression of miRNAs from peripheral blood mononuclear cells from subjects that met clinical and histopathologic criteria for sarcoidosis were compared to those from matched controls in the ACCESS study...
August 16, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28800254/sirt1-protects-against-systemic-sclerosis-related-pulmonary-fibrosis-by-decreasing-pro-inflammatory-and-pro-fibrotic-processes
#2
Haiyan Chu, Shuai Jiang, Qingmei Liu, Yanyun Ma, Xiaoxia Zhu, Minrui Liang, Xiangguang Shi, Weifeng Ding, Xiaodong Zhou, Hejian Zou, Feng Qian, Philip W Shaul, Li Jin, Jiucun Wang
Pulmonary fibrosis is the leading cause of death in systemic sclerosis (SSc). Sirtuin1 (SIRT1) is a deacetylase with known anti-inflammatory and anti-fibrotic activity in the liver, kidney and skin. The role of SIRT1 in SSc-related pulmonary fibrosis is unknown. In the present work, we determined that the expression of SIRT1 in peripheral blood mononuclear cells of SSc patients with pulmonary fibrosis is lower than that in SSc patients without pulmonary fibrosis. In in vivo studies of Bleomycin-induced lung fibrosis in mice, SIRT1 activation with Resveratrol reduced collagen production when it was administered either prophylactically during the inflammatory stage or after the development of fibrosis...
August 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28800253/targeting-pulmonary-endothelial-hemoglobin-%C3%AE-improves-nitric-oxide-signaling-and-reverses-pulmonary-artery-endothelial-dysfunction
#3
Roger A Alvarez, Megan P Miller, Scott A Hahn, Joseph C Galley, Eileen Bauer, Timothy Bachman, Jian Hu, John Sembrat, Dmitry Goncharov, Ana L Mora, Mauricio Rojas, Elena Goncharova, Adam C Straub
RATIONALE: Pulmonary hypertension is characterized by pulmonary endothelial dysfunction. Previous work showed that systemic artery endothelial cells express hemoglobin α to control nitric oxide diffusion, but the role of this system in the pulmonary circulation has not been evaluated. OBJECTIVES: We hypothesize that up-regulation of hemoglobin α in pulmonary endothelial cells contributes to nitric oxide depletion and pulmonary vascular dysfunction in pulmonary hypertension...
August 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28799781/microrna-29c-prevents-pulmonary-fibrosis-by-regulating-epithelial-cell-renewal-and-apoptosis
#4
Ting Xie, Jiurong Liang, Yan Geng, Ningshan Liu, Adrianne Kurkciyan, Vrishika Kulur, Dong Leng, Nan Deng, Zhenqiu Liu, Jianbo Song, Peter Chen, Paul W Noble, Dianhua Jiang
Successful repair and renewal of alveolar epithelial cells are critical in prohibiting the accumulation of myofibroblasts in pulmonary fibrogenesis. MicroRNAs (miRNAs) are multi-focal regulators involved in lung injury and repair. But the contribution of miRNAs to AEC2 renewal and apoptosis is incompletely understood. We report that microRNA-29c (MiR-29c) expression is lower in AEC2s of individuals with idiopathic pulmonary fibrosis (IPF) than healthy lungs. Epithelial cells overexpressing miR-29c show higher proliferative rate and viability...
August 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28787175/targeted-has2-expression-lessens-airway-responsiveness-in-chronic-murine-allergic-airway-disease
#5
Julia K L Walker, Barbara S Theriot, Michael Ghio, Carol S Trempus, Jordan E Wong, Victoria L McQuade, Jiurong Liang, Dianhua Jiang, Paul W Noble, Stavros Garantziotis, Monica Kraft, Jennifer L Ingram
RATIONALE: Hyaluronan (HA), a major component of extracellular matrix, is secreted by airway structural cells. For example, airway fibroblasts in allergic asthma secrete elevated levels of HA in association with increased hyaluronan synthase 2 (HAS2) expression. Thus, we hypothesized that HA accumulation in the airway wall may contribute to airway remodeling and hyperresponsiveness in allergic airways disease. METHODS: Transgenic mice were generated in which the smooth muscle α-actin (αSMA) promoter drives HAS2 expression...
August 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28763253/alda-1-protects-against-acrolein-induced-acute-lung-injury-and-endothelial-barrier-dysfunction
#6
Qing Lu, Miles Mundy, Eboni Chambers, Thilo Lange, Julie Newton, Diana Borgas, Hongwei Yao, Gaurav Choudhary, Rajshekhar Basak, Mahogany Oldham, Sharon Rounds
Inhalation of acrolein, a highly reactive aldehyde, causes lung edema. The underlying mechanism is poorly understood and there is no effective treatment. In this study, we demonstrated that acrolein not only dose-dependently induced lung edema, but also promoted lipopolysaccharide (LPS)-induced acute lung injury (ALI). Importantly, acrolein-induced lung injury were prevented and rescued by Alda-1, an activator of mitochondrial aldehyde dehydrogenase (ALDH) 2. Acrolein also dose-dependently increased monolayer permeability, disrupted adherens junctions and focal adhesion complexes, and caused intercellular gap formation in primary cultured lung microvascular endothelial cells (LMVEC); effects that were attenuated by Alda-1 and the antioxidant, N-acetylcysteine, but not by the NADPH inhibitor, apocynin...
August 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28723225/preferential-generation-of-15-hete-pe-induced-by-il-13-regulates-goblet-cell-differentiation-in-human-airway-epithelial-cells
#7
Jinming Zhao, Yoshinori Minami, Emily Etling, John M Coleman, Sarah N Lauder, Victoria Tyrrell, Maceler Aldrovandi, Valerie O'Donnell, Hans-Erik Claesson, Valerian Kagan, Sally Wenzel
RATIONALE: Type-2-associated goblet cell hyperplasia and mucus hypersecretion are well known features of asthma. 15-Lipoxygenase (15LO1) is induced by the Type-2 cytokines/IL-13 in human airway epithelial cells (HAEC) in vitro and is increased in fresh asthmatic HAECs ex vivo. 15LO1 generates a variety of products, including 15-hydroxyeicosatetraenoic acid (15-HETE), 15-HETE-phosphatidyethanoloamine (PE) (15-HETE-PE) and 13-hydroxyoctadecadienoic acid (13-HODE). The current study investigated the 15LO1 metabolite profile at baseline and after IL-13 treatment, and the influence on goblet cell differentiation in HAECs...
July 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28708434/epithelial-cells-induce-a-cyclooxygenase-1-dependent-endogenous-reduction-in-airway-smooth-muscle-contractile-phenotype
#8
Michael J O'Sullivan, Elizabeth Gabriel, Alice Panariti, Chan Y Park, Gijs Ijpma, Jeffrey J Fredberg, Anne-Marie Lauzon, James G Martin
Airway smooth muscle (ASM) cells are phenotypically regulated to exist in either a proliferative or a contractile state. However the influence of other airway structural cell types on ASM cell phenotype is largely unknown. Although epithelial cells are known to drive ASM proliferation, their effects on the contractile phenotype are uncertain. In the current study we tested the hypothesis that epithelial cells reduce the contractile phenotype of ASM cells. To do so, we measured force production by traction microscopy, gene and protein expression as well as calcium release by Fura-2 ratiometric imaging...
July 14, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28708422/epithelial-sodium-channel-enac-is-a-modifier-of-the-long-term-non-progressive-phenotype-associated-with-f508del-cftr-mutations
#9
Pankaj B Agrawal, Ruobing Wang, Hongmei Lisa Li, Klaus Schmitz-Abe, Chantelle Simone-Roach, Jingxin Chen, Jiahai Shi, Tin Louie, Shaohu Sheng, Meghan C Towne, Christine F Brainson, Michael A Matthay, Carla F Kim, Michael Bamshad, Mary J Emond, Norma P Gerard, Thomas R Kleyman, Craig Gerard
BACKGROUND: Cystic Fibrosis (CF) remains the most lethal genetic disease in the Caucasian population. However, there is great variability of clinical phenotype and survival, even among patients harboring the same genotype. We identified five CF patients with a homozygous F508del mutation in the CFTR gene living in their 5th or 6th decade of life, all with minimal change in lung function over longitudinal period of more than 20 years. Because of the rarity of this long-term non-progressive phenotype, we hypothesized those individuals may carry rare genetic variants in modifier genes that ameliorate disease severity...
July 14, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28707978/immunomodulatory-cell-therapy-to-target-cystic-fibrosis-inflammation
#10
Oula Khoury, Christopher Barrios, Victor Ortega, Anthony Atala, Sean V Murphy
Cystic fibrosis (CF) is associated with exaggerated and prolonged inflammation in the lungs, which contributes to lung injury, airway mucus obstruction, bronchiectasis and loss of lung function. This hyper-inflammatory phenotype appears to be caused by an imbalance between the pro- and anti-inflammatory regulatory pathways, with heightened pro-inflammatory stimuli, a decreased counter-regulatory response, and reduced effectiveness of immune cell function and inflammatory resolution. Thus, therapies that can target this inflammatory environment would have a major impact in preventing the progression of lung disease...
July 14, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28700253/house-dust-mite-induced-allergic-airway-disease-is-independent-of-ige-and-fc%C3%A9-ri%C3%AE
#11
Christopher G McKnight, Joseph A Jude, Zhenqi Zhu, Reynold A Panettieri, Fred D Finkelman
IgE contributes to disease exacerbations but not to baseline airway hyperresponsiveness (AHR) in human asthma. In rodent allergic airway disease (AAD), mast cell and IgE dependence for the induction of AHR has only been observed when mice are immunized with a relatively weak allergen without adjuvant. To evaluate the role of IgE in murine AAD that is induced by a potent allergen, we inoculated BALB/c and FVB/N background wild-type, and IgE- or FcεRIα-deficient mice intratracheally with large or limiting doses of house dust mite extract (HDM) and evaluated AHR, pulmonary eosinophilia, goblet cell metaplasia, serum IgE, and lung mastocytosis...
July 12, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28683207/loss-of-vascular-cd34-results-in-increased-sensitivity-to-lung-injury
#12
Bernard C Lo, Matthew J Gold, Sebastian Scheer, Michael R Hughes, Jessica Cait, Erin Debruin, Fanny S F Chu, David C Walker, Hesham Soliman, Fabio M Rossi, Marie-Renée Blanchet, Georgia Perona-Wright, Colby Zaph, Kelly M McNagny
Survival during lung injury requires a coordinated program of damage limitation and rapid repair. CD34 is a cell surface sialomucin expressed by epithelial, vascular and stromal cells that promotes cell adhesion, coordinates inflammatory cell recruitment, and drives angiogenesis. To test whether CD34 also orchestrates pulmonary damage and repair, we induced acute lung injury in wild type (WT) and Cd34-/- mice by bleomycin (BLM) administration. We found that Cd34-/- mice displayed severe weight loss and early mortality compared to WT controls...
July 6, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28679058/pharmacological-inhibition-of-mtor-kinase-reverses-right-ventricle-remodeling-and-improves-right-ventricle-structure-and-function-in-rats
#13
Andressa Pena, Ahasanul Kobir, Dmitry Goncharov, Akiko Goda, Tatiana V Kudryashova, Arnab Ray, Rebecca Vanderpool, Jeffrey Baust, Baojun Chang, Ana L Mora, John Gorcsan Iii, Elena A Goncharova
Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling, increased pulmonary artery pressure (PAP), right heart afterload and death. Mechanistic target of rapamycin (mTOR) promotes smooth muscle cell proliferation, survival and pulmonary vascular remodeling via two functionally distinct complexes, mTORC1 (supports cell growth) and mTORC2 (promotes cell survival), and dual mTORC1/mTORC2 inhibition selectively induces PAH PAVSMC apoptosis and reverses pulmonary vascular remodeling...
July 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28678521/restoration-of-megalin-mediated-clearance-of-alveolar-protein-as-a-novel-therapeutic-approach-for-acute-lung-injury
#14
Christine U Vohwinkel, Yasmin Buchäckert, Hamza M Al-Tamari, Luciana C Mazzocchi, Holger K Eltzschig, Konstantin Mayer, Rory E Morty, Susanne Herold, Werner Seeger, Soni S Pullamsetti, István Vadász
Acute respiratory distress syndrome (ARDS) constitutes a significant disease burden with regard to both morbidity and mortality. Current therapies are mostly supportive and do not address the underlying pathophysiologic mechanisms. Removal of protein-rich alveolar edema - a clinical hallmark of ARDS - is critical for survival. Here, we describe a TGFβ-triggered mechanism, in which megalin, the primary mediator of alveolar protein transport, is negatively regulated by GSK3β, with protein phosphatase 1 (PP1) and nuclear inhibitor of PP1 being involved in the signaling cascade...
July 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28678519/intermittent-hypoxia-and-hypercapnia-accelerate-atherosclerosis-partially-via-trimethylamine-oxide
#15
Jin Xue, Dan Zhou, Orit Poulsen, Toshihiro Imamura, Yu-Hsin Hsiao, Travis H Smith, Atul Malhotra, Pieter Dorrestein, Rob Knight, Gabriel G Haddad
RATIONALE: Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and hypercapnia (IHC) during sleep. OSA has been shown as a risk factor for atherosclerosis but the relation of IHC to induction or progression of atherosclerosis is not well understood. To dissect the mechanisms involved, we compared atherosclerotic formation between two mouse models, i.e., the apolipoprotein E (ApoE) and the low density lipoprotein receptor (Ldlr) deficient mice, with or without IHC exposure...
July 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28665693/critical-role-of-irak-m-in-regulating-antigen-induced-airway-inflammation
#16
Mingqiang Zhang, Wei Chen, Weixun Zhou, Yan Bai, Jinming Gao
Asthma is an airway epithelium disorder involving allergic lung inflammation. IRAK-M is a negative regulator of Toll-like receptor (TLR) signaling on airway epithelial cells and macrophages and known to limit overproduction of cytokines during the inflammatory process. However, the direct role of IRAK-M on asthma pathogenesis is unclear. In the present study, we found significant elevation of IRAK-M expression in mouse lungs following ovalbumin (OVA) exposure. Compared to wild type (WT) mice, IRAK-M knockout (KO) mice responded to OVA challenge with significantly worse infiltration of airway inflammatory cells, greater airway responsiveness, higher proinflammatory cytokine levels in lung homogenates, and more prominent Th2 and Th17 deviation...
June 30, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28657795/p38-mapk-inhibition-improves-heart-function-in-pressure-loaded-right-ventricular-hypertrophy
#17
Baktybek Kojonazarov, Tatyana Novoyatleva, Mario Boehm, Chris Happe, Zaneta Sibinska, Xia Tian, Amna Sajjad, Himal Luitel, Guido Posern, Steven M Evans, Friedrich Grimminger, Hossein A Ghofrani, Norbert Weissmann, Harm J Bogaard, Werner Seeger, Ralph T Schermuly
While p38 MAPK is known to have a role in ischemic heart disease and many other diseases, its contribution to the pathobiology of right ventricular (RV) hypertrophy and failure is unclear. Therefore, we sought to investigate the role of p38 MAPK to the pathophysiology of pressure overload-induced RV hypertrophy and failure. Measurements and Main Results The effects of the p38 MAPK inhibitor PH797804 were investigated in mice with RV hypertrophy/failure caused by exposure to hypoxia or pulmonary artery banding (PAB); in addition, the effects of p38 MAPK inhibition or depletion (by small interfering RNA) were studied in isolated mouse RV fibroblasts...
June 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28657777/epithelial-deletion-of-sulf2-exacerbates-bleomycin-induced-lung-injury-inflammation-and-mortality
#18
Xinping Yue
Epithelial injury has been proposed to be the initiating factor in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We have shown previously that heparan sulfate (HS) 6-O-endosulfatase 2 (Sulf2) is overexpressed in the hyperplastic type II alveolar epithelial cells (AECs) in the IPF lungs. By removing 6-O-sulfates from specific HS intra-chain sites, Sulf2 modulates the functions of many growth factors and cytokines. In this study we hypothesized that Sulf2 plays a regulatory role in alveolar epithelial injury and repair, using the murine bleomycin model...
June 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28613919/hypercapnia-accelerates-adipogenesis-a-novel-role-of-high-co2-in-exacerbating-obesity
#19
Ryota Kikuchi, Takao Tsuji, Osamu Watanabe, Kazuhiro Yamaguchi, Kinya Furukawa, Hiroyuki Nakamura, Kazutetsu Aoshiba
Obesity is a major risk factor for the development of obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS), which manifest as intermittent hypercapnia and sustained plus intermittent hypercapnia, respectively. In this study, we investigated whether CO2 affects adipocyte differentiation (adipogenesis) and maturation (hypertrophy). Human visceral or subcutaneous preadipocytes were grown to confluence and then induced to differentiate to adipocytes under hypocapnia, normocapnia, and hypercapnia with or without hypoxia...
June 14, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28613916/human-cd8-t-cells-damage-non-infected-epithelial-cells-during-influenza-virus-infection-in-vitro
#20
Carolien E van de Sandt, Montserrat Bárcena, Abraham J Koster, Jennifer Kasper, Charles J Kirkpatrick, Dana P Scott, Rory D de Vries, Susanne Herold, Guus F Rimmelzwaan, Thijs Kuiken, Kirsty R Short
During severe influenza A virus (IAV) infections a large amount of damage to the pulmonary epithelium is the result of the anti-viral immune response. Specifically, whilst CD8+ T cells are important for killing IAV-infected cells, during a severe IAV infection they can damage uninfected epithelial cells. At present, the mechanisms by which this occurs are unclear. Here, we used a novel in vitro co-culture model of human NCl-H441 cells and CD8+ T cells in order to provide a new insight into how CD8+ T cells may affect uninfected epithelial cells during severe IAV infections...
June 14, 2017: American Journal of Respiratory Cell and Molecular Biology
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