5,763 results match your criteria American Journal of Respiratory Cell and Molecular Biology[Journal]


LPS-Induced Lung Platelet Recruitment Occurs Independently from Neutrophils, PSGL-1, and P-selectin.

Am J Respir Cell Mol Biol 2019 Feb 15. Epub 2019 Feb 15.

King's College London, Pharmaceutical Sciences, London, United Kingdom of Great Britain and Northern Ireland ;

Platelets are recruited to inflammatory foci and contribute to host defence and inflammatory responses. Compared to platelet recruitment in hemostasis and thrombosis, the mechanisms of platelet recruitment in inflammation and host defence are poorly understood. Neutrophil recruitment to lung airspaces following inhalation of bacterial LPS requires platelets and PSGL-1 in mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0182OCDOI Listing
February 2019

TGFβ1 - A Novel Cause of Resistance to Bronchodilators in Asthma?

Am J Respir Cell Mol Biol 2019 Feb 15. Epub 2019 Feb 15.

Imperial College, Respiratory Pharmacology, London, United Kingdom of Great Britain and Northern Ireland ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2019-0020EDDOI Listing
February 2019
1 Read

"Ion" the Prize - Defining the Complexities of Airway Epithelial Cell Ion Transport Functions.

Am J Respir Cell Mol Biol 2019 Feb 15. Epub 2019 Feb 15.

McMaster University, 3710, Firestone Institute for Respiratory Health, Hamilton, Ontario, Canada ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0414EDDOI Listing
February 2019

Mesenchymal Cells and Bronchopulmonary Dysplasia: New Insights about the Dark Side of Oxygen.

Authors:
Antonia P Popova

Am J Respir Cell Mol Biol 2019 Feb 15. Epub 2019 Feb 15.

University of Michigan, Department of Pediatrics, Ann Arbor, Michigan, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2019-0010EDDOI Listing
February 2019

Converging Paths of Pulmonary Arterial Hypertension and Cellular Senescence.

Am J Respir Cell Mol Biol 2019 Feb 13. Epub 2019 Feb 13.

University Medical Center Groningen, Center for Congenital Heart Diseases, Groningen, Netherlands.

Cellular senescence is recognized as a crucial contributor to the pathobiology of various degenerative and cardiovascular diseases, like idiopathic pulmonary fibrosis and atherosclerosis. We describe the potential link between cellular senescence and the degenerative character of neointimal pulmonary vascular disease in pulmonary arterial hypertension (PAH). Senescence markers have been described in remodeled pulmonary arteries, triggers that induce senescence also induce PAH, pathways known to be disturbed in PAH, such as TGFβ/BMP and TNFα, are also causally associated to senescence and interventions that target a senescence phenotype, also target pulmonary vascular remodeling in vivo. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0329TRDOI Listing
February 2019
1 Read

A Flow Cytometric Method for Isolating Cystic Fibrosis Airway Macrophages from Expectorated Sputum.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

University of Washington School of Medicine, 12353, Pulmonary, Critical Care, and Sleep Medicine, Seattle, Washington, United States.

Research to understand the contribution of macrophages to non-resolving airway inflammation in cystic fibrosis (CF) and other chronic suppurative airways diseases has been hindered by a lack of methods for isolating and studying theses cells. With the development of technologies that can characterize small numbers of cells or individual cells, there is an even greater need for methodologies to isolate rare cells in heterogeneous specimens. Here, we describe a method that overcomes the technical obstacles imposed by sputum debris and apoptotic cells, and allows isolation of pure populations of macrophages from CF sputum. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0236MADOI Listing
February 2019
1 Read

Pendrin Mediates Bicarbonate Secretion and Enhances CFTR Function in Airway Surface Epithelia.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

McGill University, Physiology, Montreal, Quebec, Canada.

Bicarbonate facilitates mucin unpacking and bacterial killing however its transport mechanisms in the airways are not well understood. cAMP stimulates anion efflux through the CFTR (ABCC7) anion channel and this is defective in CF. The anion exchanger pendrin (SLC26A4) also mediates HCO3- efflux and is upregulated by proinflammatory cytokines. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0158OCDOI Listing
February 2019
1 Read

Metabolic Adaptation Supports Persistent Methicillin-Resistant Staphylococcus aureus Pulmonary Infection.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

Columbia University, Pediatrics, New York, New York, United States ;

Rationale: Methicillin-resistant Staphylococcus aureus (MRSA) is a versatile human pathogen associated with diverse types of infections, ranging from benign colonization to sepsis. We postulated that MRSA must undergo specific genotypic and phenotypic changes to cause chronic pulmonary disease.

Objectives: We investigated how MRSA adapts to the human airway to establish chronic infection, as occurs during cystic fibrosis (CF). Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0389OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0389OCDOI Listing
February 2019
3 Reads

Prolonged Cold-Ischemia Induces Necroptotic Cell Death in Ischemia Reperfusion Injury and Contributes to Primary Graft Dysfunction After Lung Transplantation.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

University of Pittsburgh, Pittsburgh, Pennsylvania, United States.

Primary graft dysfunction (PGD), a major cause of morbidity after lung transplantation, is linked to ischemia-reperfusion injury (IRI). Other factors such as preceding brain death (BD), hemorrhagic shock (HS), and pre-engraftment lung management are also important. We hypothesized that a multi-hit isogenic mouse model of lung transplantation is more closely linked to PGD than IRI alone. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0207OCDOI Listing
February 2019
1 Read

TGF-β1 Decreases β2-Agonist-Induced Relaxation in Human Airway Smooth Muscle.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

Rutgers Robert Wood Johnson Medical School, 12287, Medicine, Piscataway, New Jersey, United States.

Helper T effector cytokines implicated in asthma modulate the contractility of human airway smooth muscle (HASM) cells. We have reported recently that a profibrotic cytokine, transforming growth factor beta 1 (TGF-β1), induces HASM cell shortening and airway hyper-responsiveness (AHR). Here we assessed whether TGF-β1 affects the ability of HASM cells to relax in response to β2-agonists, a mainstay treatment for AHR in asthma. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0301OCDOI Listing
February 2019
1 Read

PPARγ Deficiency Exacerbates Fibrotic Response to Mycobacteria Peptide in Murine Sarcoidosis Model.

Am J Respir Cell Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

East Carolina University, Dept of Internal Medicine, Greenville, North Carolina, United States ;

We established a murine model of multiwall carbon nanotube (MWCNT)-elicited chronic granulomatous disease which bears similarities to human sarcoidosis pathology including alveolar macrophage deficiency of peroxisome-proliferator-activated receptor gamma (PPARγ). Because lymphocyte reactivity to mycobacterial antigens has been reported in sarcoidosis, we hypothesized that addition of mycobacterial Early Secreted Antigenic Target Protein 6 (ESAT-6) to MWCNT might exacerbate pulmonary granulomatous pathology. MWCNT with or without ESAT-6 peptide-14 were instilled by oropharyngeal route into macrophage-specific PPARγ KO or wild-type mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0346OCDOI Listing
February 2019
1 Read

End-Stage Takes Center Stage in PAH.

Am J Respir Cell Mol Biol 2019 Feb 6. Epub 2019 Feb 6.

Vanderbilt University School of Medicine, Pediatrics, Pediatric Pulmonary Medicine, Nashville, Tennessee, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2019-0022EDDOI Listing
February 2019
1 Read

Vaping Away Epithelial Integrity.

Authors:
Rohit Gaurav

Am J Respir Cell Mol Biol 2019 Feb 6. Epub 2019 Feb 6.

National Jewish Health, Department of Pediatrics, Denver, Colorado, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2019-0016EDDOI Listing
February 2019
3.985 Impact Factor

An Elusive Fox that Suppresses Scgb1a1 in Asthma Has Been Found.

Am J Respir Cell Mol Biol 2019 Feb 6. Epub 2019 Feb 6.

University of Rochester, Pediatrics, Rochester, New York, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2019-0019EDDOI Listing
February 2019

February Highlights/Papers by Junior Investigators/NIH News.

Authors:

Am J Respir Cell Mol Biol 2019 Feb;60(2):ii

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.602iiDOI Listing
February 2019

Attenuation of Allergen, IL-13- and TGF-α-Induced Lung Fibrosis Following the Treatment of IL-15 in Mice.

Am J Respir Cell Mol Biol 2019 Jan 31. Epub 2019 Jan 31.

Tulane University School of Medicine, 12255, Medicine/Pulmonary, New Orleans, Louisiana, United States ;

Rationale: Endogenous IL-15-deficiency promotes lung fibrosis; therefore, we examined the effect of induced IL-15 in restricting the progression of lung fibrosis.

Objective: Establish a novel therapeutic molecule for pulmonary fibrosis Method. Western blot, qPCR and ELISA analyses were performed on the lung tissues of IL-15-deficient mice, rIL-15 treated CC-10-IL-13, CC10-TGF-α mice, and allergen-challenged CC10-IL-15 mice were examined to establish the anti-fibrotic affect of IL-15 in lung fibrosis. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0254OCDOI Listing
January 2019
1 Read
3.985 Impact Factor

Genome-Wide Association Analysis of Single Breath Diffusing Capacity of Carbon Monoxide (DLCO).

Am J Respir Cell Mol Biol 2019 Jan 29. Epub 2019 Jan 29.

Channing Laboratory, Medicine, Boston, Massachusetts, United States ;

Diffusing capacity of carbon monoxide (DLCO) is a widely used pulmonary function test in clinical practice and a particularly useful measure in assessing patients with COPD. We hypothesized that elucidating genetic determinants of DLCO could lead to better understanding of the genetic architecture of COPD. We estimated the heritability of DLCO using common genetic variants and performed genome-wide association analyses in four cohorts enriched for COPD subjects (COPDGene, NETT, GenKOLS and TESRA) using a combined European-ancestry white (EA) dataset and a COPDGene African American (AA) dataset. Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0384OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0384OCDOI Listing
January 2019
5 Reads

Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure.

Am J Respir Cell Mol Biol 2019 Jan 29. Epub 2019 Jan 29.

University of Pennsylvania, Biostatistics, Epidemiology and Informatics, Philadelphia, Pennsylvania, United States ;

Glucocorticoids, commonly used asthma controller medications, decrease symptoms in most patients, but some remain symptomatic despite high dose treatment. The physiological basis underlying glucocorticoid response, especially among asthma patients with severe, refractory disease is not fully understood. We sought to identify differences between fatal asthma and non-asthma donor-derived airway smooth muscle (ASM) cell transcriptomic response to glucocorticoid exposure, and to compare ASM-specific changes to those of other cell types. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0385OCDOI Listing
January 2019

The STATus of STAT3 in Lung Cell Senescence?

Am J Respir Cell Mol Biol 2019 Jan 23. Epub 2019 Jan 23.

Centre de Recherche en Cancérologie de Lyon, UMR INSERM U1052/CNRS 5286, Lyon, France.

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2019-0013ED
Publisher Site
http://dx.doi.org/10.1165/rcmb.2019-0013EDDOI Listing
January 2019

MAP(kinase)-ing a Link Between Obesity and Inflammation in Severe Asthma.

Authors:
Amanda L Tatler

Am J Respir Cell Mol Biol 2019 Jan 23. Epub 2019 Jan 23.

University of Nottingham, Respiratory Medicine , Nottingham, United Kingdom of Great Britain and Northern Ireland ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0419EDDOI Listing
January 2019

Piezo1 in the Lung - At Last!

Am J Respir Cell Mol Biol 2019 Jan 17. Epub 2019 Jan 17.

Columbia University, Pediatrics, New York, New York, United States.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0418EDDOI Listing
January 2019
1 Read

Dietary Fatty Acids Amplify Inflammatory Responses to Infection through p38 MAP Kinase Signaling.

Am J Respir Cell Mol Biol 2019 Jan 16. Epub 2019 Jan 16.

Woolcock Institute of Medical Research, Sydney, New South Wales, Australia.

Obesity is an important risk factor for severe asthma exacerbations, which are mainly caused by respiratory infections. Dietary fatty acids, which are increased systemically in obese patients and are further increased after high fat meals, affect the innate immune system and may contribute to dysfunctional immune responses to respiratory infection. This study investigated the effects of dietary fatty acids on immune responses to respiratory infection in pulmonary fibroblasts and a bronchial epithelial cell line (BEAS-2B). Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0215OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0215OCDOI Listing
January 2019
5 Reads

What Lies Beneath: Preformed Autoantibodies and Lung Transplantation.

Am J Respir Cell Mol Biol 2019 Jan 16. Epub 2019 Jan 16.

University of Alabama at Birmingham, 9968, Pulmonary and Critical Care, Birmingham, Alabama, United States.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0415EDDOI Listing
January 2019
2 Reads

A Little Complement Goes a Long Way: A Perspective from the Pleural Space.

Authors:
Torry A Tucker

Am J Respir Cell Mol Biol 2019 Jan 15. Epub 2019 Jan 15.

University of Texas Health Science Center at Tyler, Texas Lung Injury Institute, Tyler, Texas, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0395EDDOI Listing
January 2019
1 Read

Growth Differentiation Factor (GDF)-15 in Pulmonary and Critical Care Medicine.

Am J Respir Cell Mol Biol 2019 Jan 11. Epub 2019 Jan 11.

University of Michigan Health System, Internal Medicine, Ann Arbor, Michigan, United States ;

Growth differentiation factor 15 (GDF-15) acts both as a stress-induced cytokine with diverse actions at different body sites and as a cell-autonomous regulator linked to cellular senescence and apoptosis. For multiple reasons, this divergent transforming growth factor (TGF)-β molecular superfamily member should be better known to pulmonary researchers and clinicians. In ambulatory individuals, GDF-15 concentrations in peripheral blood are an established predictive biomarker of all-cause mortality and of adverse cardiovascular events. Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0379TR
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0379TRDOI Listing
January 2019
5 Reads

Ovine Models of Congenital Heart Disease and the Consequences of Hemodynamic Alterations for Pulmonary Artery Remodeling.

Am J Respir Cell Mol Biol 2019 Jan 8. Epub 2019 Jan 8.

University of California at San Francisco, Pediatrics, San Francisco, California, United States.

The natural history of pulmonary vascular disease (PVD) associated with congenital heart disease (CHD) depends upon associated hemodynamics. Patients exposed to increased pulmonary blood flow (PBF) and pulmonary arterial pressure (PAP) develop PVD more commonly than patients exposed to increased PBF alone. To investigate the effects of these differing mechanical forces on physiologic and molecular responses, we developed two models of CHD utilizing fetal surgical techniques: 1) left pulmonary artery (LPA) ligation primarily resulting in increased PBF; and 2) aortopulmonary shunt placement resulting in increased PBF and PAP. Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0305MA
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0305MADOI Listing
January 2019
5 Reads

IL-17A-Producing γδT Cells Inhibit the Formation of Malignant Pleural Effusions.

Am J Respir Cell Mol Biol 2019 Jan 4. Epub 2019 Jan 4.

Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Department of Respiratory and Critical Care Medicine, Wuhan, China ;

γδT cells are an important source of IL-17A and play an anti- or pro-tumor role depending on the surrounding microenvironment. The precise role of γδT cells in the development of malignant pleural effusions (MPE) remains unknown. Using flow cytometry, the distribution and differentiation of γδT cells in wild-type (WT) and IL-10-⁄- mice were analyzed. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0201OCDOI Listing
January 2019
2 Reads

STAT3 Regulates the Onset of Oxidant-Induced Senescence in Lung Fibroblasts.

Am J Respir Cell Mol Biol 2019 Jan 4. Epub 2019 Jan 4.

University Drive, University of Newcastle, School of Biomedical Sciences and Pharmacy, Callaghan, New South Wales, Australia ;

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause with a median survival of only 3 years. We and others have shown that fibroblasts derived from IPF-lungs display characteristics of senescent cells and that dysregulated activation of the transcription factor signal transducer and activator of transcription 3 (STAT3) correlates with IPF progression. The question of whether STAT3 activation is involved in fibroblast senescence remains unanswered. Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0328OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0328OCDOI Listing
January 2019
6 Reads

Myocardin is Involved in Mesothelial-Mesenchymal Transition of Human Pleural Mesothelial Cells.

Am J Respir Cell Mol Biol 2019 Jan 3. Epub 2019 Jan 3.

University of Texas Health Northeast, 12341, Tyler, Texas, United States ;

Pleural fibrosis is characterized by severe inflammation of the pleural space, pleural reorganization. Subsequent thickening of visceral pleura contributes to lung stiffness and impaired lung function. Pleural mesothelial cells (PMCs) can become myofibroblasts via mesothelial-mesenchymal transition (MesoMT) and contribute to pleural organization, fibrosis and rind formation. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0121OCDOI Listing
January 2019
4 Reads

January Highlights/Papers by Junior Investigators/NIH News.

Authors:

Am J Respir Cell Mol Biol 2019 Jan;60(1)

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.601iDOI Listing
January 2019
1 Read

Old Cells in Young Airway Smooth Muscle: Does Neonatal Senescence Cause Lifelong Airway Obstruction?

Am J Respir Cell Mol Biol 2018 Dec 21. Epub 2018 Dec 21.

National Jewish Health, Medicine, Denver, Colorado, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0399EDDOI Listing
December 2018
1 Read

The Club Cell Marker SCGB1A1 Downstream of FOXA2 is Reduced in Asthma.

Am J Respir Cell Mol Biol 2018 Dec 21. Epub 2018 Dec 21.

University of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona, United States ;

Human SCGB1A1 protein has been shown to be significantly reduced in bronchoalveolar lavage, sputum and serum from human asthmatics as compared to healthy individuals. However, the mechanism of this reduction and its functional impact have not been entirely elucidated. By mining online datasets, we found that the message RNA of SCGB1A1 was significantly repressed in brushed human airway epithelial cells from asthmatics and this repression appeared to be associated with the reduced expression of FOXA2. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0199OCDOI Listing
December 2018
7 Reads

Vaporized E-Cigarette Liquids Induce Ion Transport Dysfunction in Airway Epithelia.

Am J Respir Cell Mol Biol 2018 Dec 21. Epub 2018 Dec 21.

University of Alabama at Birmingham, Department of Medicine, Gregory J. Fleming Cystic Fibrosis Center, Departments of Pediatrics and Cell Developmental and Integrative Biology, Birmingham, Alabama, United States ;

Cigarette smoking is associated with chronic obstructive pulmonary disease and chronic bronchitis. Acquired ion transport abnormalities, including CFTR dysfunction, caused by cigarette smoking have been proposed as potential mechanisms for mucus obstruction in chronic bronchitis. Although popular and perceived to be safe, it remains unclear if e-cigarette use harms the airways via mechanisms altering ion transport. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2017-0432OCDOI Listing
December 2018
3 Reads

Fatty Acid Oxidation Protects Against Hyperoxia-Induced Endothelial Cell Apoptosis and Lung Injury in Neonatal Mice.

Am J Respir Cell Mol Biol 2018 Dec 20. Epub 2018 Dec 20.

Brown University Warren Alpert Medical School, 12321, Molecular Biology, Cell Biology & Biochemistry, Providence, Rhode Island, United States.

In neonates, hyperoxia or positive pressure ventilation causes continued lung injury characterized by simplified vascularization and alveolarization, which are the hallmarks of bronchopulmonary dysplasia. Although endothelial cells (ECs) have metabolic flexibility to maintain cell function under stress, it is unknown whether hyperoxia causes metabolic dysregulation in ECs, leading to lung injury. We hypothesized that hyperoxia alters EC metabolism, which causes EC dysfunction and lung injury. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0335OCDOI Listing
December 2018
1 Read

Emphysema Associated Autoreactive Antibodies Exacerbate Post Lung Transplant Ischemia Reperfusion Injury.

Am J Respir Cell Mol Biol 2018 Dec 20. Epub 2018 Dec 20.

Medical University of South Carolina, Microbiology and Immunology, Charleston, South Carolina, United States ;

COPD-associated chronic inflammation has been shown to lead to an autoimmune phenotype characterized in part by the presence of lung reactive autoreactive antibodies. We hypothesized that ischemia reperfusion injury (IRI) liberates epitopes that would facilitate pre-existing autoantibody binding, thereby exacerbating lung injury post-transplantation. We induced emphysema in C57BL/6 mice through 6 months of cigarette smoke exposure (CS). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0224OCDOI Listing
December 2018
2 Reads

Pulmonary Neuroendocrine Cells Secrete GABA to Induce Goblet Cell Hyperplasia in Primate Models.

Am J Respir Cell Mol Biol 2018 Dec 20. Epub 2018 Dec 20.

Brigham and Women's Hospital, Division of Pulmonary and Critical Care Medicine, Boston, Massachusetts, United States ;

Mucus overproduction is a major contributor to morbidity and mortality in asthma. Mucus overproduction is induced by orchestrated actions of multiple factors that include inflammatory cytokines and γ-aminobutyric acid (GABA). GABA is produced only by pulmonary neuroendocrine cells (PNECs) in the mouse lung. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0179OCDOI Listing
December 2018
2 Reads

Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness.

Am J Respir Cell Mol Biol 2018 Dec 18. Epub 2018 Dec 18.

Brigham and Women's Hospital, Medicine | Pulmonary, Boston, Massachusetts, United States ;

Rationale: Altered expression of syndecan-2, a heparan sulfate proteoglycan, has been associated with diverse types of human cancers. However, the mechanisms by which syndecan-2 may contribute to the pathobiology of lung adenocarcinoma have not been previously explored.

Methods: Syndecan-2 levels were measured in human lung adenocarcinoma samples and Lung Cancer Tissue Microarrays using immunohistochemistry and real time-PCR. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0118OCDOI Listing
December 2018
1 Read

Stretch-Activated Piezo1 Channel in Endothelial Cells Relaxes Mouse Intrapulmonary Arteries.

Am J Respir Cell Mol Biol 2018 Dec 18. Epub 2018 Dec 18.

Universite de Bordeaux, 27086, Talence, Aquitaine, France.

In intrapulmonary artery (IPA), endothelial cells (EC) respond to mechanical stimuli by releasing vasoactive factors to set the vascular tone. Piezo1, a stretch-activated calcium permeable channel is a sensor of mechanical stress in EC. The present study was undertaken to investigate the implication of Piezo1 in the endothelium-dependent regulation of IPA tone and its potential involvement in pulmonary hypertension, the main disease of this circulation. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0197OCDOI Listing
December 2018
1 Read

Oxygen Disrupts Human Fetal Lung Mesenchymal Cells: Implications for Bronchopulmonary Dysplasia.

Am J Respir Cell Mol Biol 2018 Dec 18. Epub 2018 Dec 18.

Ottawa Hospital Research Institute & CHEO Research Institute, Pediatrics, Ottawa, Ontario, Canada ;

Rationale And Objectives: Exogenous mesenchymal stromal cells ameliorate experimental bronchopulmonary dysplasia. Moreover, data from term-born animal models and human tracheal aspirate-derived cells suggests altered mesenchymal signaling pathways in the pathophysiology of neonatal lung disease. Here, we sought to determine if tissue-resident human fetal lung mesenchymal cells contribute to normal and oxygen-impaired lung development, thus linking endogenous mesenchymal (dys-)function and exogenous mesenchymal cell repair activity. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0358OCDOI Listing
December 2018
2 Reads

"Yap"-ing about the Antifibrotic Benefits of Prostacyclin.

Authors:
Steven K Huang

Am J Respir Cell Mol Biol 2018 Dec 18. Epub 2018 Dec 18.

University of Michigan, Pulmonary and Critical Care Medicine, Ann Arbor, Michigan, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0392EDDOI Listing
December 2018
1 Read

Advancing Chronic Obstructive Pulmonary Disease Therapy: Opportunities, Challenges, and Excitement.

Am J Respir Cell Mol Biol 2019 Jan;60(1):1-2

1 IMED Biotech Unit AstraZeneca Cambridge, United Kingdom and.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0288EDDOI Listing
January 2019
1 Read

Systems Analysis of the Human Pulmonary Arterial Hypertension Lung Transcriptome.

Am J Respir Cell Mol Biol 2018 Dec 18. Epub 2018 Dec 18.

Indiana University School of Medicine, 12250, Medicine, Indianapolis, Indiana, United States.

Rationale: Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary artery pressure and vascular resistance, typically leading to right heart failure and death. Current therapies improve quality of life of the patients but have a modest effect on long-term survival. A detailed transcriptomics and systems biology view of the PAH lung is expected to provide new testable hypotheses for exploring novel treatments. Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0368OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0368OCDOI Listing
December 2018
11 Reads

Intracellular Heat Shock Protein 70 Deficiency in Pulmonary Fibrosis.

Am J Respir Cell Mol Biol 2018 Dec 13. Epub 2018 Dec 13.

Medical University of South Carolina, Medicine, Charleston, South Carolina, United States.

Idiopathic Pulmonary Fibrosis (IPF) pathogenesis has been postulated to involve a variety of mechanisms associated with the aging process, including loss of protein homeostasis (proteostasis). Heat shock proteins (Hsp) are cellular chaperones that serve a number of vital maintenance and repair functions, including the regulation of proteostasis. Previously published data have implicated Hsp70 in the development of pulmonary fibrosis in animal models. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2017-0268OCDOI Listing
December 2018
1 Read

Another Weapon in the Battle Against Idiopathic Pulmonary Fibrosis?

Am J Respir Cell Mol Biol 2018 Dec 12. Epub 2018 Dec 12.

University of Washington, Medicine, Division of Pulmonary Critical Care, Seattle, Washington, United States.

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0387ED
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0387EDDOI Listing
December 2018
1 Read

The Tyrosine Kinase Inhibitor TAS-115 Attenuates Bleomycin-Induced Lung Fibrosis in Mice.

Am J Respir Cell Mol Biol 2018 Dec 12. Epub 2018 Dec 12.

University of Tokushima Graduate School, Respiratory Medicine and Rheumatology, Tokushima, Japan ;

The signaling pathways of growth factors including platelet-derived growth factor (PDGF) can be considered specific targets for overcoming the poor prognosis of idiopathic pulmonary fibrosis (IPF). Nintedanib, the recently approved multiple kinase inhibitor, has shown promising anti-fibrotic effects in IPF patients; however, its efficacy is still limited, and in some cases, treatment discontinuation is necessary due to toxicities such as gastrointestinal disorders. Therefore, more effective agents with less toxicity are still needed. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0098OCDOI Listing
December 2018
2 Reads

The Antifibrotic Activity of Prostacyclin Receptor Agonism is Mediated through Inhibition of YAP/TAZ.

Am J Respir Cell Mol Biol 2018 Dec 11. Epub 2018 Dec 11.

Idorsia Pharmaceuticals Ltd, 510456, Cardiovascuklar and Fibrosis Biology, Allschwil, Switzerland ;

Idiopathic pulmonary fibrosis (IPF) is a life-threatening progressive disease characterized by loss of alveolar epithelial cells, inflammation and aberrant fibroblast activation. The two currently approved therapies do not halt or reverse tissue remodeling and therefore novel disease modifying mechanisms are needed. Our results describe YAP/TAZ inhibition through IP receptor activation as a novel mechanism that suppresses pro-fibrotic (myo)fibroblast activity. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0142OCDOI Listing
December 2018
3 Reads

Hyperoxia-Induced Cellular Senescence in Fetal Airway Smooth Muscle Cells.

Am J Respir Cell Mol Biol 2018 Dec 3. Epub 2018 Dec 3.

Mayo Clinic College of Medicine and Science, 12270, Department of Anesthesiology and Perioperative Medicine, Rochester, Minnesota, United States.

Supplemental O2 (hyperoxia; 30-90% O2) is a necessary intervention for premature infants, but contributes to development of neonatal and pediatric asthma, necessitating better understanding of contributory mechanisms in hyperoxia-induced changes to airway structure and function. In adults, environmental stressors promote formation of senescent cells that secrete factors (senescence-associated secretory phenotype; SASP), which can be inflammatory and have paracrine effects that enhance chronic lung diseases. Hyperoxia-induced changes in airway structure and function are mediated in part by effects on airway smooth muscle (ASM). Read More

View Article

Download full-text PDF

Source
https://www.atsjournals.org/doi/10.1165/rcmb.2018-0176OC
Publisher Site
http://dx.doi.org/10.1165/rcmb.2018-0176OCDOI Listing
December 2018
14 Reads

Drugging the Mighty Neutrophil in COPD.

Am J Respir Cell Mol Biol 2018 Dec 3. Epub 2018 Dec 3.

NIEHS/NIH, LRB, Research Triangle Park, North Carolina, United States ;

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2018-0370EDDOI Listing
December 2018
1 Read