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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/29345973/r-spondin-2-is-upregulated-in-idiopathic-pulmonary-fibrosis-and-affects-fibroblasts-behavior
#1
Adrián Munguía-Reyes, Yalbi I Balderas-Martínez, Carina Becerril, Marco Checa, Remedios Ramírez, Blanca Ortíz-Quintero, Jorge Meléndez-Zajgla, Annie Pardo, Moisés Selman
Idiopathic pulmonary fibrosis (IPF) is characterized by the expansion of the myofibroblasts population, excessive extracellular matrix accumulation, and destruction of the lung parenchyma. The R-spondins family (RSPO) comprises a group of proteins essential for development. From them, RSPO2 is expressed primarily in the lungs and its mutations cause severe defects in the respiratory tract. Interestingly, RSPO2 participates in the canonical WNT pathway, a critical route in the pathogenesis of IPF. Thus, the aim of this study was to examine the expression and putative role of RSPO2 in this disease...
January 18, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29337590/novel-mechanism-for-nicotinamide-phosphoribosyltransferase-inhibition-of-tnf-%C3%AE-mediated-apoptosis-in-human-lung-endothelial-cells
#2
Radu C Oita, Sara M Camp, Wenli Ma, Ermelinda Ceco, Mark Harbeck, Patrick Singleton, Joe Messana, Xiaoguang Sun, Ting Wang, Joe G N Garcia
Nicotinamide phosphoribosyltransferase (NAMPT) exists as both intracellular (iNAMPT) and extracellular (eNAMPT) proteins. eNAMPT is secreted into the blood and functions as a cytokine/enzyme (cytozyme) that activates NFκB signaling via ligation of the TLR4 receptor, further serving as a biomarker for inflammatory lung disorders such as the acute respiratory distress syndrome (ARDS). In contrast, iNAMPT is involved in nicotinamide mononucleotide (NMN) synthesis and has been implicated in the regulation of cellular apoptosis, although the exact mechanisms for this regulation are poorly understood...
January 16, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29314868/bronchiolitis-obliterans-and-pulmonary-fibrosis-after-sulfur-mustard-inhalation-in-rats
#3
Matthew D McGraw, Marilyn M Dysart, Tara B Hendry-Hofer, Paul R Houin, Jacqueline S Rioux, Rhonda B Garlick, Joan E Loader, Russell Smith, Danielle C Paradiso, Wesley W Holmes, Dana R Anderson, Carl W White, Livia A Veress
RATIONALE: Inhalation of powerful chemical agents, such as sulfur mustard (SM), can have debilitating pulmonary consequences, such as bronchiolitis obliterans (BO) and parenchymal fibrosis (PF). The underlying pathogenesis of disorders after SM inhalation is not clearly understood, resulting in a paucity of effective therapies. OBJECTIVE: To evaluate the role of pro-fibrotic pathways involving TGF-β and PDGF in the development of BO and PF after inhalation injury sustained by SM, using a rat model...
January 9, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29314865/il-17-plays-a-role-in-rsv-induced-lung-inflammation-and-emphysema-in-elastase-and-lps-injured-mice
#4
Yohannes A Mebratu, Yohannes Tesfaigzi
Respiratory syncytial virus (RSV) is associated with enhanced progression of chronic obstructive pulmonary disease (COPD) and COPD exacerbations. However, little is known about the role of IL-17 in RSV-induced lung injury. We first investigated the role of RSV infection in enhancing mucous cell hyperplasia and airspace enlargement in the lungs of mice injured with elastase and lipopolysaccharide (E/LPS). Mice injured with E/LPS had an enhanced and prolonged neutrophilic response to RSV that was associated with decreased levels of type I IFN and increased levels of IL-17, IL-23, CXCL-1, GCSF and CXCL-5 and MMP-9...
January 9, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29314863/bacterial-derived-neutrophilic-inflammation-drives-lung-remodeling-in-a-mouse-model-of-copd
#5
Bradley W Richmond, Rui-Hong Du, Wei Han, John T Benjamin, Riet van der Meer, Linda Gleaves, Marshall Guo, Austin McKissack, Yongqin Zhang, Dong-Sheng Cheng, Vasiliy V Polosukhin, Timothy S Blackwell
Loss of secretory immunoglobulin A (SIgA) is common in the small airways of patients with chronic obstructive pulmonary disease (COPD) and may contribute to disease pathogenesis. Using mice that lack SIgA in the airways due to genetic deficiency of polymeric immunoglobulin receptor (pIgR-/- mice), we investigated the role of neutrophils in driving the fibrotic small airway wall remodeling and emphysema that develops spontaneously in these mice. By flow cytometry, we found an increase in the percentage of neutrophils among CD45+ cells in the lungs, as well as an increase in total neutrophils, in pIgR-/- mice compared to wild-type (WT) controls...
January 9, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29268036/no-independent-sgc-activation-improves-vascular-function-and-cardiac-remodeling-in-sickle-cell-disease
#6
Karin P Potoka, Katherine C Wood, Jeffrey J Baust, Marta Bueno, Scott A Hahn, Rebecca R Vanderpool, Tim Bachman, Grace M Mallampalli, David O Osei-Hwedieh, Valerie Schrott, Bin Sun, Grant C Bullock, Eva-Maria Becker-Pelster, Matthias Wittwer, Jan Stampfuss, Ilka Mathar, Johannes-Peter Stasch, Hubert Truebel, Peter Sandner, Ana L Mora, Adam C Straub, Mark T Gladwin
Sickle cell disease (SCD) is associated with intravascular hemolysis and oxidative inhibition of nitric oxide (NO) signaling. BAY 54-6544 is a small molecule activator of oxidized sGC; which unlike endogenous NO and the sGC stimulator BAY 41-8543; preferentially binds and activates heme-free, NO-insensitive sGC to restore enzymatic cGMP production. We tested orally delivered sGC activator BAY 54-6544, sGC stimulator BAY 41-8543, sildenafil, or placebo for 4-12 weeks in a transgenic mouse model of SCD (BERK-SCD) and their hemizygous littermate controls (BERK-Hemi)...
December 21, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29268030/inhibition-of-macrophage-complement-receptor-crig-by-trim72-polarizes-innate-immunity-of-the-lung
#7
Nagaraja Nagre, Xiaofei Cong, César Terrazas, Ian Pepper, John M Schreiber, Hongyun Fu, Joshua M Sill, John W Christman, Abhay R Satoskar, Xiaoli Zhao
[Rationale] The complement system plays a critical role in immune responses against pathogens. However, its identity and regulation in the lung are not fully understood. [Objectives] This study aims to explore the role of tripartite motif protein 72 (TRIM72) in regulating complement receptor (CR) of the immunoglobulin superfamily (CRIg) in alveolar macrophage (AM) and innate immunity of the lung. [Methods] Imaging, absorbance quantification and flow cytometry were used to evaluate in vitro and in vivo AM phagocytosis with normal, or altered, TRIM72 expression...
December 21, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29262264/pde8-is-expressed-in-human-airway-smooth-muscle-and-selectively-regulates-camp-signaling-by-%C3%AE-2ar-ac6
#8
Timothy B Johnstone, Kaitlyn H Smith, Cynthia J Koziol-White, Fengying Li, Austin G Kazarian, Maia L Corpuz, Maya Shumyatcher, Frederick J Ehlert, Blanca E Himes, Reynold A Panettieri, Rennolds S Ostrom
Two cAMP signaling compartments centering around adenylyl cyclase (AC) exist in human airway smooth muscle (HASM) cells, one containing ß2AR-AC6 and another containing E prostanoid receptors (EPR)-AC2. We hypothesized that different phosphodiesterase (PDE) isozymes selectively regulate cAMP signaling in each compartment. According to RNA-seq data, 18 of 24 PDE genes were expressed in primary HASM cells derived from age- and gender-matched donors with and without asthma. PDE8A was the third most abundant of the cAMP-degrading PDE genes, after PDE4A and PDE1A...
December 20, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29256623/identification-of-drug-candidates-to-suppress-cigarette-smoke-induced-inflammation-via-cmap-analyses
#9
Gilles Vanderstocken, Anna Dvorkin-Gheva, Pamela Shen, Corry-Anke Brandsma, Ma'en Obeidat, Yohan Bossé, John A Hassell, Martin R Stampfli
Cigarette smoking is the main risk factor for COPD, and to date, existing pharmacologic interventions have been ineffective at controlling inflammatory processes associated with the disease. To address this issue, we used the Connectivity Map (cMap) database to identify drug candidates with the potential to attenuate cigarette smoke-induced inflammation. We queried cMap using three independent, in house cohorts of healthy non-smokers and smokers. Potential drug candidates were validated against four publicly available human datasets, as well as six independent data sets from cigarette smoke-exposed mice...
December 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29232161/characterization-of-novel-missense-variants-of-serpina1-gene-causing-alpha-1-antitrypsin-deficiency
#10
Nerea Matamala, Beatriz Lara, Gema Gomez-Mariano, Selene Martínez, Diana Retana, Taiomara Fernandez, Ramona Angeles Silvestre, Irene Belmonte, Francisco Rodriguez-Frias, Marçal Vilar, Raquel Sáez, Igor Iturbe, Silvia Castillo, María Molina-Molina, Anna Texido, Gema Tirado-Conde, Jose Luis Lopez-Campos, Manuel Posada, Ignacio Blanco, Sabina Janciauskiene, Beatriz Martinez-Delgado
SERPINA1 gene is highly polymorphic, with more than one hundred variants described in databases. The SERPINA1 encodes alpha-1 antitrypsin (AAT) protein, and the severe deficiency of AAT is a major contributor to pulmonary emphysema and liver diseases. We report seven new variants in Spanish patients with AAT deficiency. All variants involved amino acid substitutions in different exons: PiSDonosti (S+Ser14Phe), PiTijarafe (Ile50Asn), PiSevilla (Ala58Asp), PiCadiz (Glu151Lys), PiTarragona (Phe227Cys), PiPuerto Real (Thr249Ala) and PiValencia (Lys328Glu)...
December 12, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29220578/pd-1-pd-l1-pathway-mediates-the-alleviation-of-pulmonary-fibrosis-by-human-mesenchymal-stem-cells-in-humanized-mice
#11
Ke Ni, Ming Liu, Jian Zheng, Liyan Wen, Qingyun Chen, Zheng Xiang, Kowk-Tai Lam, Yinping Liu, Godfrey Chi-Fung Chan, Yu-Lung Lau, Wenwei Tu
RATIONALE: Pulmonary fibrosis is a chronic progressive lung disease with few treatments. Human mesenchymal stem cells (MSC) have been shown to be beneficial to pulmonary fibrosis as they have the immunomodulatory capacity. However, there is no reliable model to test the therapeutic effect of human MSC in vivo. METHODS: Here, to mimic pulmonary fibrosis in humans, we established a novel bleomycin-induced pulmonary fibrosis model in humanized mice. Based on this model, the benefit of human MSC to pulmonary fibrosis and underlying mechanism were investigated...
December 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29216437/epha2-modulation-associates-with-protective-effect-of-prone-position-in-ventilator-induced-lung-injury
#12
Byung Hoon Park, Mi Hwa Shin, Ivor S Douglas, Kyung Soo Chung, Joo Han Song, Song Yee Kim, Eun Young Kim, Ji Ye Jung, Young Ae Kang, Joon Chang, Young Sam Kim, Moo Suk Park
The erythropoietin-producing hepatoma receptor tyrosine kinase A2 (EphA2) and its ligand ephrinA1 play a pivotal role in inflammation and tissue injury by modulating the epithelial and endothelial barrier integrity. Therefore, EphA2 receptor may be a potential therapeutic target for modulating ventilator-induced lung injury (VILI). To support this hypothesis, here we analyzed EphA2/ephrinA1 signaling in the process of VILI and determined the role of EphA2/ephrinA1 signaling in the protective mechanism of prone positioning in a VILI model...
December 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29211497/the-rho-kinase-isoforms-rock1-and-rock2-each-contribute-to-the-development-of-experimental-pulmonary-fibrosis
#13
Rachel S Knipe, Clemens K Probst, David Lagares, Alicia Franklin, Jillian J Spinney, Patricia L Brazee, Paula Grasberger, Linlin Zhang, Katharine E Black, Norihiko Sakai, Barry S Shea, James K Liao, Benjamin D Medoff, Andrew M Tager
Pulmonary fibrosis is thought to result from dysregulated wound repair after repetitive lung injury. Many cellular responses to injury involve rearrangements of the actin cytoskeleton mediated by the two isoforms of the Rho-associated coiled coil forming protein kinase, ROCK1 and ROCK2. Additionally, profibrotic mediators such as transforming growth factor-beta (TGF-β), thrombin and lysophosphatidic acid (LPA) act through receptors that activate ROCK. Inhibition of ROCK activation may be a potent therapeutic strategy for human pulmonary fibrosis...
December 6, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29206476/systemic-markers-of-adaptive-and-innate-immunity-are-associated-with-copd-severity-and-spirometric-disease-progression
#14
Eitan Halper-Stromberg, Jeong H Yun, Margaret M Parker, Ruth Tal Singer, Amit Gaggar, Edwin K Silverman, Sonia Leach, Russell P Bowler, Peter J Castaldi
The progression of chronic obstructive pulmonary disease (COPD) is associated with marked alterations in circulating immune cell populations, but no studies have characterized alterations in these cell types across the full spectrum of lung function impairment in current and former smokers. In 6,299 subjects from the COPDGene and ECLIPSE studies, we related Coulter blood counts and proportions to cross-sectional FEV1 adjusting for current smoking status. We also related cell count measures to three-year change in FEV1 in ECLIPSE subjects...
December 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29206475/whole-blood-gene-expression-in-pulmonary-non-tuberculous-mycobacterial-infection
#15
Steven A Cowman, Joseph Jacob, David M Hansell, Peter Kelleher, Robert Wilson, William O C Cookson, Miriam F Moffatt, Michael R Loebinger
RATIONALE: The factors predisposing towards the development of pulmonary non-tuberculous mycobacterial disease (pNTM) and influencing disease progression remain unclear. Impaired immune responses have been reported in individuals with pNTM but data are limited and inconsistent. OBJECTIVES: To use gene expression profiling to examine the host response to pNTM. METHODS: Microarray analysis of whole blood gene expression was performed on 25 subjects with pNTM and 27 uninfected controls with respiratory disease...
December 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29190429/gene-edited-mle-15-cells-as-a-model-for-the-hermansky-pudlak-syndromes
#16
Seunghyi Kook, Aidong Qi, Ping Wang, Shufang Meng, Peter Gulleman, Lisa R Young, Susan H Guttentag
Defining the mechanisms of cellular pathogenesis for rare lung diseases such as Hermansky Pudlak syndrome (HPS) is often complicated by loss of the differentiated phenotype of cultured primary alveolar type 2 (AT2) cells, and by a lack of durable cell lines that are faithful to both AT2 cell and rare disease phenotypes. We used CRISPR/Cas9 gene editing to generate a series of HPS-specific mutations in the MLE-15 cell line. The resulting MLE-15/HPS cell lines exhibit preservation of AT2 cellular functions, including formation of lamellar body-like organelles, complete processing of Surfactant protein B (SP-B), and known features of HPS specific to each trafficking complex, including loss of protein targeting to lamellar bodies...
November 30, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29182484/ppar%C3%AE-regulates-mitochondrial-structure-and-function-and-hpasmc-proliferation
#17
Samantha M Yeligar, Bum-Yong Kang, Kaiser M Bijli, Jennifer M Kleinhenz, Tamara C Murphy, Gloria Torres, Alejandra San Martin, Roy L Sutliff, C Michael Hart
Pulmonary hypertension (PH) is a progressive disorder that causes significant morbidity and mortality despite existing therapies. PH pathogenesis is characterized by metabolic derangements that increase pulmonary artery smooth muscle cell (PASMC) proliferation and vascular remodeling. PH-associated decreases in peroxisome proliferator-activated receptor gamma (PPARγ) stimulate PASMC proliferation, and PPARγ in coordination with PPARγ coactivator 1 alpha (PGC1α) regulates mitochondrial gene expression and biogenesis...
November 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29141155/neutrophil-mediated-suppression-of-influenza-induced-pathology-requires-cd11b-cd18-mac-1
#18
Tamar Tak, Tomasz P Rygiel, Guruswamy Karnam, Okan W Bastian, Louis Boon, Marco Viveen, Frank E Coenjaerts, Linde Meyaard, Leo Koenderman, Janesh Pillay
Severe influenza virus infection can lead to life-threatening pathology through immune-mediated tissue damage. In various experimental models, this damage is dependent on T-cells. There is conflicting evidence regarding the role of neutrophils in influenza-mediated pathology. Neutrophils are often regarded as cells causing tissue damage, but in recent years it has become clear that a subset of human neutrophils is capable of suppressing T-cells, which is dependent on Mac-1 (CD11b/CD18). Therefore, we tested the hypothesis that immune suppression by neutrophils can reduce T-cell mediate pathology after influenza infection...
November 15, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29115860/lysyl-oxidase-like-1-protein-deficiency-protects-mice-from-adtgf-%C3%AE-1-induced-pulmonary-fibrosis
#19
Pierre-Simon Bellaye, Chiko Shimbori, Chandak Upagupta, Seidai Sato, Wei Shi, Jack Gauldie, Kjetil Ask, Martin Kolb
Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterised by excessive deposition of extracellular matrix (ECM) in the lung parenchyma. The abnormal ECM deposition slowly overtakes normal lung tissue disturbing gas-exchange and leading to respiratory failure and death. ECM cross-linking and subsequent stiffening is thought to be a major contributor of disease progression and also promotes the activation of TGF-β1, one of the main pro-fibrotic growth factors. Lysyl oxidase-like1 (LOXL1) belongs to the crosslinking enzyme family and has been shown to be upregulated in active fibrotic regions of bleomycin-treated mice and IPF patients...
November 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29115856/lps-induced-acute-lung-injury-involves-the-nf-%C3%AE%C2%BAb-mediated-downregulation-of-sox18
#20
Christine M Gross, Manuela Kellner, Ting Wang, Qing Lu, Xutong Sun, Evgeny A Zemskov, Satish Noonepalle, Archana Kangath, Sanjiv Kumar, Manuel Gonzalez-Garay, Ankit A Desai, Saurabh Aggarwal, Boris Gorshkov, Christina Klinger, Alexander D Verin, John D Catravas, Jeffrey R Jacobson, Jason X-J Yuan, Ruslan Rafikov, Joe G N Garcia, Stephen M Black
One of the early events in the progression of lipopolysaccharide (LPS)-mediated acute lung injury (ALI) in mice is the disruption of the pulmonary endothelial barrier resulting in lung edema. However, the molecular mechanisms by which the endothelial barrier becomes compromised remain unresolved. The SRY-related High Mobility Group box (Sox) group-F family member, Sox18, is a barrier- protective protein through its ability to increase the expression of the tight junction protein, Claudin-5. Thus, the purpose of this study was to determine if down-regulation of the Sox18-Claudin-5 axis plays a role in the pulmonary endothelial barrier disruption associated with LPS exposure...
November 8, 2017: American Journal of Respiratory Cell and Molecular Biology
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