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    4818 results match your criteria American Journal of Physiology - Lung Cellular and Molecular Physiology[Journal]

    1 OF 97

    MK2 mediates macrophage activation and acute lung injury by regulating let-7e miRNA.
    Am J Physiol Lung Cell Mol Physiol 2018 May 17. Epub 2018 May 17.
    Shanghai Jiao Tong University, China.
    MAPK-activated protein kinase 2 (MK2) plays a critical role in the development of inflammation. However, the modulatory mechanisms in macrophage activation and acute lung injury (ALI) haven't been completely defined. Here, we reported that MK2 deficient mice (MK2-/-) protected against sepsis-induced ALI. Read More

    Pannexin 1 channels on endothelial cells mediate vascular inflammation during lung ischemia-reperfusion injury.
    Am J Physiol Lung Cell Mol Physiol 2018 May 10. Epub 2018 May 10.
    Surgery, University of Virginia, United States.
    Ischemia-reperfusion injury (IRI), which involves inflammation, vascular permeability, and edema, remains a major challenge after lung transplantation. Pannexin 1 (Panx1) channels modulate cellular ATP release during inflammation. This study tests the hypothesis that endothelial Panx1 is a key mediator of vascular inflammation and edema after IR and that IRI can be blocked by Panx1 antagonism. Read More

    Treatment of rat congenital diaphragmatic hernia with sildenafil and NS-304, selexipag's active compound, at the pseudoglandular stage improves lung vasculature.
    Am J Physiol Lung Cell Mol Physiol 2018 May 10. Epub 2018 May 10.
    Pediatric Surgery/Cell Biology, Erasmus MC, Netherlands.
    Patients with congenital diaphragmatic hernia (CDH) often suffer from severe pulmonary hypertension and the choice of current vasodilator therapy is mostly based on trial and error. Since pulmonary vascular abnormalities are already present early during development, we performed a study to modulate these pulmonary vascular changes at an early stage during gestation. Pregnant Sprague-Dawley rats were treated with nitrofen at day 9. Read More

    Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543.
    Am J Physiol Lung Cell Mol Physiol 2018 May 10. Epub 2018 May 10.
    Pediatrics, Stanford University, United States.
    Pulmonary artery smooth muscle cells (PASMC) express endothelin (ET-1) which modulates the pulmonary vascular response to hypoxia. Although cross-talk between hypoxia-inducible factor-1α (HIF-1α), an O-sensitive transcription factor, and ET-1 is established, the cell-specific relationship between HIF-1α and ET-1 expression remains incompletely understood. We tested the hypotheses that in PASMC: (i) HIF-1α expression constrains ET-1 expression; and (ii) a specific microRNA (miRNA) links HIF-1α and ET-1 expression. Read More

    Changes in the pattern of fibrosis in the rat lung with repetitive orotracheal instillations of gastric contents: Evidence of persistent collagen accumulation.
    Am J Physiol Lung Cell Mol Physiol 2018 May 10. Epub 2018 May 10.
    Department of Respiratory Diseases and Medical Research Center, Pontificia Universidad Católica de Chile, Chile.
    Recurrent aspiration of gastric contents has been associated with several interstitial lung diseases. Despite this association, the pathogenic role of aspiration in these diseases has been poorly studied and little is known about extracellular matrix (ECM) changes in animal models of repetitive events of aspiration. Our aim was to study the repair phase of lung injury induced by each of several instillations of gastric fluid in Sprague-Dawley rats to evaluate changes in ECM and their reversibility. Read More

    AMD3100 ameliorates cigarette smoke-induced emphysema-like manifestations in mice.
    Am J Physiol Lung Cell Mol Physiol 2018 May 10. Epub 2018 May 10.
    Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, United States.
    We have shown that cigarette smoke (CS)-induced pulmonary emphysema-like manifestations are preceded by marked suppression of the number and function of bone marrow hematopoietic progenitor cells (HPC). To investigate if a limited availability of HPC may contribute to CS-induced lung injury, we used an FDA-approved antagonist of the interactions of SDF-1 with its receptor CXCR4 to promote intermittent HPC mobilization and tested its ability to limit emphysema-like injury following chronic CS. We administered AMD3100 (5mg/kg) to mice during a chronic CS exposure protocol of up to 24 weeks. Read More

    Alveolar epithelial cell processing of nanoparticles activates autophagy and lysosomal exocytosis.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Department of Medicine, University of Southern California, United States.
    Utilizing confocal microscopy, we quantitatively assessed uptake, processing and egress of near infrared (NIR)-labeled carboxylated polystyrene nanoparticles (PNP) in live alveolar epithelial cells (AEC) during interactions with primary rat AEC monolayers (RAECM). PNP fluorescence intensity (content) and colocalization with intracellular vesicles in a cell were determined over the entire cell volume via z-stacking. Isotropic cuvette-based microfluorimetry was used to determine PNP concentration ([PNP]) from anisotropic measurements of PNP content assessed by confocal microscopy. Read More

    Inhibition of Raf1 ameliorates bleomycin-induced pulmonary fibrosis through attenuation of TGFβ1 signaling.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Medicine, University of Pittsburgh, United States.
    Idiopathic Pulmonary Fibrosis (IPF) is a fatal fibrotic lung disease associated with aberrant activation and differentiation of fibroblasts, leading to abnormal extracellular matrix (ECM) production. Currently, it is still an untreatable disease except lung transplantation. Here, we demonstrate that the Raf1 inhibitor GW5074 ameliorates lung fibrosis in bleomycin-induced pulmonary fibrosis. Read More

    MMP-12 activates protease activated receptor (PAR)-1, upregulates placenta growth factor and leads to pulmonary emphysema.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    National Taiwan University, Taiwan.
    Due to the expansion of aging and smoking populations, chronic pulmonary obstructive disease (COPD) is predicted to be the third leading cause of death worldwide in 2030. It is therefore pertinent to develop effective therapy to improve management for COPD. Cigarette smoke-mediated protease-antiprotease imbalance is a major pathogenic mechanism for COPD and results in massive pulmonary infiltration of neutrophils and macrophages, releasing excessive neutrophil elastase (NE) and matrix metalloproteinases (MMPs). Read More

    Long-term Culture and Cloning of Primary Human Bronchial Basal Cells that Maintain Multipotent Differentiation Capacity and CFTR Channel Function.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Cell Biology, UT Southwestern Medical Center, United States.
    While primary cystic fibrosis (CF) and non-CF human bronchial epithelial basal cells (HBECs) accurately represent in vivo phenotypes, one barrier to their wider use has been a limited ability to clone and expand cells in sufficient numbers to produce rare genotypes using genome editing tools. Recently, conditional reprogramming of cells (CRC) with a ROCK inhibitor and culture on an irradiated fibroblast feeder layer resulted in extension of the lifespan of HBECs, but differentiation capacity and CF transmembrane conductance regulator (CFTR) function decreased as a function of passage. This report details modifications to the standard HBEC CRC protocol (Mod CRC), including the use of bronchial epithelial growth medium instead of F-medium and 2% oxygen instead of 21% oxygen, that extend HBEC lifespan while preserving multipotent differentiation capacity and CFTR function. Read More

    Damage-Associated Molecular Patterns (DAMPs) in Resuscitated Hemorrhagic Shock Are Mitigated by Peritoneal Fluid Administration.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Surgery, University of Louisville.
    Introduction: Conventional resuscitation (CR) of hemorrhagic shock (HS), a significant cause of trauma mortality, is I.V. blood and fluids. Read More

    NMDA receptor activation inhibits the anti-fibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Central South University Xiangya Medical School, China.
    Endogenous glutamate (Glu) release and N-methyl-D-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation and tissue-protection, play a protective role in pulmonary fibrosis (PF) process. Read More

    The role of non-coding RNAs in regulating epithelial responses in COPD.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    University of New South Wales, Australia.
    Chronic obstructive pulmonary disease (COPD), one of the leading causes of death in the world, is a chronic inflammatory disease of the airways usually caused by long-term exposure to inhaled irritants. Airway epithelial cells (AECs) play a key role in initializing COPD and driving the exacerbation of this disease through the release of various cytokines. This AEC-derived cytokine response is tightly regulated possibly through the regulatory effects of non-coding RNAs (ncRNAs). Read More

    Intrauterine growth restriction decreases nuclear factor-kappa B signaling in fetal pulmonary artery endothelial cells of fetal sheep.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Pediatrics, Stanford University, United States.
    Intrauterine growth restriction (IUGR) in premature newborns increases the risk for bronchopulmonary dysplasia (BPD), a chronic lung disease characterized by disrupted pulmonary angiogenesis and alveolarization. We previously showed that experimental IUGR impairs angiogenesis, however, mechanisms that impair pulmonary artery endothelial cell (PAEC) function are uncertain. The nuclear factor-kappa-B (NFκB) pathway promotes vascular growth in the developing mouse lung, and we hypothesized that IUGR disrupts NFκB-regulated pro-angiogenic targets in fetal PAEC. Read More

    miR-142-3p is associated with aberrant Wingless/Integrase I (WNT) signaling during airway remodeling in asthma.
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    Internal Medicine, University of Giessen and Marburg Lung Center (UGMLC), Germany.
    Background: Asthma is characterized by a chronic inflammation and remodeling of the airways. While inflammation can be controlled, therapeutic options to revert remodeling do not exist. Thus, there is a large and unmet need to understand the underlying molecular mechanisms in order to develop novel therapies. Read More

    Is fibroblast growth factor signaling pathway a victim of receptor tyrosine kinase inhibition in pulmonary parenchymal and vascular remodeling?
    Am J Physiol Lung Cell Mol Physiol 2018 May 3. Epub 2018 May 3.
    University of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Germany.
    Idiopathic pulmonary arterial hypertension (IPAH), pulmonary hypertension (PH) due to lung disease and/or hypoxia and idiopathic pulmonary fibrosis (IPF) are increasingly recognized as important contributors to mortality and morbidity worldwide. Among others, the current treatment paradigm considers broad inhibition of receptor tyrosine kinases, a strategy that likely leads to collateral inhibition of signaling pathways that are critical for lung repair and regeneration. Fibroblast growth factor 7 (FGF7) and FGF10 signaling in the lung through FGF receptor 2 (FGFR2) are involved in epithelial cell protection and renewal, and mutations in their corresponding genes in humans are linked to increased susceptibility to lung pathologies such as chronic obstructive pulmonary disease and bronchopulmonary dysplasia. Read More

    FABP4 regulates eosinophil recruitment and activation in allergic airway inflammation.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 26. Epub 2018 Apr 26.
    University of Minnesota, United States.
    Fatty acid binding protein 4 (FABP4), a member of a family of lipid-binding proteins, is known to play a role in inflammation by virtue of its ability to regulate intracellular events such as lipid fluxes and signaling. Studies have indicated a pro-inflammatory role for FABP4 in allergic asthma, although its expression and function in eosinophils, the predominant inflammatory cells recruited to allergic airways, was not investigated. We examined expression of FABP4 in murine eosinophils and its role in regulating cell recruitment in vitro as well as in cockroach antigen (CRA)-induced allergic airway inflammation. Read More

    Fibroblast senescence in the pathology of idiopathic pulmonary fibrosis.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 26. Epub 2018 Apr 26.
    The University of Newcastle Australia, Australia.
    Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneumonia of unknown cause with a median survival of only 3 years. Little is known about the mechanisms that precede the excessive collagen deposition seen in IPF, but cellular senescence has been strongly implicated in disease pathology. Senescence is a state of irreversible cell cycle arrest accompanied by an abnormal secretory profile and is thought to play a critical role in both development and wound repair. Read More

    Effects of budesonide and surfactant in preterm, fetal sheep.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 19. Epub 2018 Apr 19.
    Pediatrics-Neonatology, Saint Louis University, United States.
    Background: Mechanical ventilation causes lung injury and systemic inflammatory responses in preterm sheep, and is associated with bronchopulmonary dysplasia (BPD) in preterm infants. Budesonide added to surfactant decreased BPD by 20% in infants.

    Objective: Determine the effects of budesonide and surfactant on injury from high tidal volume (VT) ventilation in preterm lambs. Read More

    Neuropilin-2 regulates airway inflammatory responses to inhaled lipopolysaccharide.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 19. Epub 2018 Apr 19.
    Pediatrics, University of North Carolina School of Medicine, United States.
    Neuropilins are multifunctional receptors that play important roles in immune regulation. Neuropilin-2 (NRP2) is expressed in the lungs, but whether it regulates airway immune responses is unknown. Here, we report that Nrp2 is weakly expressed by alveolar macrophages (AM) in the steady-state, but is dramatically up-regulated following in vivo lipopolysaccharide (LPS) inhalation. Read More

    PAI-1 is a novel component of the miR-17~92 signaling that regulates pulmonary artery smooth muscle cell phenotypes.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 12. Epub 2018 Apr 12.
    Pediatrics, University of Illinois at Chicago, United States.
    We have previously reported that miR-17~92 is critically involved in the pathogenesis of pulmonary hypertension (PH). We also identified two novel mR-17/20a direct targets PDLIM5 and PHD2 and elucidated the signaling pathways by which PDLIM5 and PHD2 regulate functions of pulmonary artery smooth muscle cells (PASMC). In addition, we have shown that plasminogen activator inhibitor-1 (PAI-1) is also downregulated in PASMC that overexpress miR-17~92. Read More

    β1 Subunit of the Calcium-Sensitive Potassium Channel Modulates the Pulmonary Vascular Smooth Muscle Cell Response to Hypoxia.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 12. Epub 2018 Apr 12.
    Pediatrics, Stanford University, United States.
    Accessory subunits associated with the calcium-sensitive potassium channel (BK), a major determinant of vascular tone, confer functional and anatomical diversity. The β1 subunit increases Ca-, and voltage-sensitivity of the BK channel and is expressed exclusively in smooth muscle cells (SMC). Evidence supporting the physiologic significance of the β1 subunit includes the observations that murine models with deletion of the β1 subunit are hypertensive and that humans with a gain-of-function β1 mutation are at decreased risk of diastolic hypertension, However, whether the β1 subunit of the BK channel contributes to the low tone that characterizes the normal pulmonary circulation or modulates the pulmonary vascular response to hypoxia remains unknown. Read More

    Decreased epithelial and sputum miR-221-3p associates with airway eosinophilic inflammation and CXCL17 expression in asthma.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 12. Epub 2018 Apr 12.
    Department of Internal Medicine, Tongji Hospital, Huazhong University of Science and Technology, China.
    Airway eosinophilic inflammation is a key feature of type 2-high asthma. The role of epithelial miRNA in airway eosinophilic inflammation remains unclear. We examined the expression of miR-221-3p in bronchial brushings, induced sputum and plasma from 77 symptomatic, recently diagnosed steroid-naïve subjects with asthma and 36 healthy controls by quantitative PCR, and analyzed the correlation between miR-221-3p expression and airway eosinophilia. Read More

    Activation of the NFkB pathway alters the phenotype of MSCs in the tracheal aspirates of preterm infants with severe BPD.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 12. Epub 2018 Apr 12.
    Department of General Pediatrics and Neonatology, University Hospital of Giessen and Marburg, Giessen (UGMLC), Germany.
    Mesenchymal stromal cells (MSCs) are released into the airways of preterm infants following lung injury. These cells display a pro-inflammatory phenotype and are associated with development of severe bronchopulmonary dysplasia (BPD). We aimed to characterize the functional properties of MSCs obtained from tracheal aspirates of 50 preterm infants who required invasive ventilation. Read More

    Recent developments in 3D reconstruction and stereology to study the pulmonary vasculature.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 12. Epub 2018 Apr 12.
    Institute of Functional and Applied Anatomy, Hannover Medical School, Germany.
    Alterations of the pulmonary vasculature are an important feature of human lung diseases such as chronic obstructive pulmonary disease, pulmonary hypertension and bronchopulmonary dysplasia. Experimental studies to investigate the pathogenesis or a therapeutic intervention in animal models of these diseases often require robust, meaningful and efficient morphometric data that allow for appropriate statistical testing. The gold standard for obtaining such data is design-based stereology. Read More

    Carbonic anhydrase IX is a critical determinant of pulmonary microvascular endothelial cell pH regulation and angiogenesis during acidosis.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 5. Epub 2018 Apr 5.
    Physiology and Cell Biology and Medicine, Center for Lung Biology, University of South Alabama, United States.
    Carbonic anhydrase IX (CA IX) is highly expressed in rapidly proliferating and highly glycolytic cells, where it serves to enhance acid regulatory capacity. Pulmonary microvascular endothelial cells (PMVECs) actively utilize aerobic glycolysis and acidify media while pulmonary arterial endothelial cells (PAECs) primarily rely on oxidative phosphorylation and minimally change media pH. Therefore, we hypothesized that CA IX is critical to PMVEC angiogenesis due to its important role in regulating pH. Read More

    The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity.
    Am J Physiol Lung Cell Mol Physiol 2018 Apr 5. Epub 2018 Apr 5.
    Univ. of Iowa College of Med., HHMI, United States.
    Mainstay therapeutics are ineffective in some people with asthma, suggesting a need for additional agents. In the current study, we used vagal ganglia transcriptome profiling and connectivity mapping to identify compounds beneficial for alleviating airway hyperreactivity. As a comparison, we also utilized previously published transcriptome data from sensitized mouse lungs and human asthmatic endobronchial biopsies. Read More

    Maternal PUFA omega-3 supplementation prevents hyperoxia-induced pulmonary hypertension in the offspring.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 29. Epub 2018 Mar 29.
    EA 4489 - Perinatal Environment and Health, Univ.Lille, CHU Lille, France.
    Pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) affect 16-25% of premature infants with bronchopulmonary dysplasia (BPD), contributing significantly to perinatal morbidity and mortality. Polyunsaturated fatty acids ω-3 (PUFA ω-3) can improve vascular remodeling, angiogenesis, and inflammation under pathophysiological conditions. However, the effects of PUFA ω-3 supplementation in BPD-associated PH are unknown. Read More

    Developmental Differences in Focal Adhesion Kinase Expression Modulate Pulmonary Endothelial Barrier Function in Response to Inflammation.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 29. Epub 2018 Mar 29.
    Pediatrics, Stanford University, United States.
    Compromised pulmonary endothelial cell (PEC) barrier function characterizes acute respiratory distress syndrome (ARDS), a cause of substantial morbidity and mortality. Survival from ARDS is greater in children compared to adults. Whether developmental differences intrinsic to PEC barrier function contribute to this survival advantage remains unknown. Read More

    Ablation of the Leptin receptor in Myeloid Cells Impairs Pulmonary Clearance of Streptococcus Pneumoniae and Alveolar Macrophage Bactericidal Function.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 22. Epub 2018 Mar 22.
    Internal Medicine, University of Michigan.
    Leptin is a pleiotropic hormone produced by white adipose tissue that regulates appetite and many physiologic functions including the immune response to infection. Genetic leptin deficiency in humans and mice impairs host defenses against respiratory tract infections. Since leptin deficiency is associated with obesity and other metabolic abnormalities, we generated mice that lack the leptin receptor (LepRb) in cells of the myeloid linage (LysM-LepRb-KO) to evaluate its impact in lean metabolically normal mice in a murine model of pneumococcal pneumonia. Read More

    The relationship between complement C3 expression and the MUC5B genotype in pulmonary fibrosis.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 22. Epub 2018 Mar 22.
    Department of Medicine, University of Colorado, United States.
    The common gain-of-function MUC5B promoter variant (rs35705950) is the strongest risk factor for the development of idiopathic pulmonary fibrosis (IPF). While the role of complement in IPF is controversial, both MUC5B and the complement system play a role in lung host defense. The aim of this study was to evaluate the relationship between C3 and MUC5B in patients with IPF and in bleomycin-induced lung injury in mice. Read More

    Calcitonin gene-related peptide hyperpolarizes mouse pulmonary artery endothelial tubes through KATP channel activation.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 15. Epub 2018 Mar 15.
    Medical Pharmacology and Physiology, University of Missouri - Columbia, United States.
    The sensory neurotransmitter calcitonin gene-related peptide (CGRP) is associated with vasodilation of systemic arteries through activation of ATP-sensitive potassium channels (KATP) in smooth muscle cells (SMCs), however its effects on endothelial cell (EC) membrane potential (Vm) are unresolved. In pulmonary arteries (PAs) of C57BL/6J mice, we questioned whether CGRP would hyperpolarize ECs as well as SMCs. Intact PAs were isolated and immunostained for CGRP to confirm sensory innervation; vessel segments (length, 1-2 mm; diameter ∼150 µm) with intact or denuded endothelium were cannulated and pressurized to 16 cm H2O at 37{degree sign}C. Read More

    Nintedanib reduces pulmonary fibrosis in a model of rheumatoid arthritis-associated interstitial lung disease.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 15. Epub 2018 Mar 15.
    Program in Cell Biology, Pediatrics, National Jewish Health, United States.
    Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) develops in approximately 20% of patients with RA. SKG mice, which are genetically prone to developing autoimmune arthritis, develop a pulmonary interstitial pneumonia that resembles human cellular and fibrotic non-specific interstitial pneumonia. Nintedanib, a tyrosine kinase inhibitor approved for the treatment of idiopathic pulmonary fibrosis, has been shown to reduce lung function decline. Read More

    Neuropilin-1and platelet-derived growth factor receptors cooperatively regulate intermediate filaments and mesenchymal cell migration during alveolar septation.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 15. Epub 2018 Mar 15.
    Internal Medicine, University of Iowa Carver College of Medicine.
    Secondary alveolar septa are mostly generated after birth in humans and in mice this is completely accomplished postnatally, when mechanical stresses vary as airspace pressure oscillates. Alveolar mesenchymal cells deposit elastic fibers which limit cellular strain, but while the elastic fiber network is incomplete, this function is also served by the intracellular cytoskeleton. Intermediate filament proteins support deformation during cellular division and migration, which occur during septal elongation. Read More

    Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 15. Epub 2018 Mar 15.
    Medicine and Anesthesia, Cardiovascular Research Institute, University of California, San Francisco, United States.
    Evidence is accumulating that exposure to cigarette smoke (CS) increases the risk of developing Acute Respiratory Distress Syndrome (ARDS). S. pneumoniae is the most common cause of bacterial pneumonia, which in turn is the leading cause of ARDS. Read More

    Time-resolved Proteome Profiling of Normal Lung Development.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 8. Epub 2018 Mar 8.
    Pacific Northwest National Laboratory, United States.
    Biochemical networks mediating normal lung morphogenesis and function have important implications for ameliorating morbidity and mortality in premature infants. While several transcript-level studies have examined normal lung development, corresponding protein-level analyses are lacking. Here we performed proteomics analysis of murine lungs from embryonic to early adult ages to identify the molecular networks mediating normal lung development. Read More

    Greater cellular stiffness in fibroblasts from patients with idiopathic pulmonary fibrosis.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 8. Epub 2018 Mar 8.
    Medical Biology, University Medical Center Groningen, Netherlands.
    Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease involving degenerative breathing capacity. Fibrotic disease is driven by dysregulation in mechanical forces at the organ, tissue and cellular level. While it is known that, in certain pathologies, diseased cells are stiffer than healthy cells, it is not known if fibroblasts derived from patients with IPF are stiffer than their normal counterparts. Read More

    Inhibiting Bruton's Tyrosine Kinase Rescues Mice from Lethal Influenza Induced Acute Lung Injury.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 8. Epub 2018 Mar 8.
    Biochemistry / Biomedical Research, The University of Texas Health Center at Tyler, United States.
    Infection with seasonal influenza A virus (IAV) leads to lung inflammation and respiratory failure, a main cause of death in influenza infected patients. Previous experiments in our laboratory indicated that Bruton's tyrosine kinase (Btk) plays a substantial role in regulating inflammation in the respiratory region during acute lung injury (ALI) in mice, therefore we sought to determine if blocking Btk activity had a protective effect in the lung during influenza induced inflammation. A Btk inhibitor (Btk Inh. Read More

    Seeing Cilia: Imaging Modalities for Ciliary Motion and Clinical Connections.
    Am J Physiol Lung Cell Mol Physiol 2018 Mar 1. Epub 2018 Mar 1.
    Department of Medicine; Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, United States.
    The respiratory tract is lined with multi-ciliated epithelial cells that function to move mucus and trapped particles via the mucociliary transport apparatus. Genetic and acquired ciliopathies result in diminished mucociliary clearance, contributing to disease pathogenesis. Recent innovations in imaging technology has advanced our understanding of ciliary motion in health and disease states. Read More

    TGF-β1-induced deposition of provisional extracellular matrix by tracheal basal cells promotes epithelial-to-mesenchymal transition in a JNK1-dependent manner.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 22. Epub 2018 Feb 22.
    Pathology, University of Vermont College of Medicine, United States.
    Epithelial cells have been suggested as potential drivers of lung fibrosis, although the epithelial-dependent pathways that promote fibrogenesis remain unknown. Extracellular matrix is increasingly recognized as an environment that can drive cellular responses in various pulmonary diseases. In this study, we demonstrate that transforming growth factor- beta (TGF-β1)-stimulated mouse tracheal basal (MTB) cells produce provisional matrix proteins in vitro, which initiate mesenchymal changes in subsequently freshly plated MTB cells via Rho kinase- and c-Jun-N-terminal kinase (JNK1)-dependent processes. Read More

    Aging and Anatomical Variations in Lung Tissue Stiffness.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 22. Epub 2018 Feb 22.
    Physiology and Biomedical Engineering, Mayo Clinic, United States.
    Lung function is inherently mechanical in nature, and depends on the capacity to conduct air and blood to and from the gas exchange regions. Variations in the elastic properties of the human lung across anatomical compartments and with aging are likely important determinants of lung function, but remain relatively poorly characterized. Here we applied atomic force microscopy to characterize human lung tissue from subjects ranging in age from 11 to 60 years old. Read More

    The atypical chemokine receptor ACKR2 drives pulmonary fibrosis by tuning influx of CCR2+ and CCR5+ IFNγ-producing γδT cells in mice.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 22. Epub 2018 Feb 22.
    Universidade Federal de Minas Gerais, Brasil.
    Rationale: Chemokines coordinate lung inflammation and fibrosis by acting on chemokine receptors expressed on leukocytes and other cell types. Atypical chemokine receptors (ACKRs) bind, internalize and degrade chemokines, tuning homeostasis and immune responses. ACKR2 recognizes and decreases levels of inflammatory CC chemokines. Read More

    Pulmonary IL-1β expression in early life causes permanent changes in lung structure and function in adulthood.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 15. Epub 2018 Feb 15.
    Department of Pediatrics, University of Gothenburg and Divison of Neonatology, Sahlgrenska University Hospital, Sweden.
    Chorioamnionitis, mechanical ventilation, oxygen therapy, and postnatal infection promote inflammation in the newborn lung. The long-term consequences of pulmonary inflammation during infancy have not been well characterized. The aim of this study was to examine the impact of inflammation during the late saccular to alveolar stages of lung development on lung structure and function in adulthood. Read More

    Inhibition of mucin secretion via glucocorticoid-induced regulation of calcium-related proteins in mouse lung.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 15. Epub 2018 Feb 15.
    College of Veterinary Medicine, Chungbuk National University, Korea (South), Republic of.
    Calcium is important for physiological functioning in many tissues and is essential in mucus secretion and muscle contraction. Intracellular concentrations of calcium are regulated by calcium-related proteins such as TRPV4, TRPV6, CaBP-9k, NCX1, and PMCA1. In this study, the relationship between secretion of pulmonary mucus and calcium regulation was investigated. Read More

    DRUG INDUCED PULMONARY ARTERIAL HYPERTENSION: A PRIMER FOR CLINICIANS AND SCIENTISTS.
    Am J Physiol Lung Cell Mol Physiol 2018 Feb 8. Epub 2018 Feb 8.
    Medicine, stanford university, United States.
    Drug-induced pulmonary arterial hypertension (D-PAH) is a form of World Health Organization (WHO) Group 1 pulmonary hypertension (PH) defined by severe small vessel loss and obstructive vasculopathy, which leads to progressive right heart failure and death. To date, 16 different compounds have been associated with D-PAH, including anorexigens, recreational stimulants, and more recently, several Food and Drug Administration (FDA)-approved medications. While the clinical manifestation, pathology, and hemodynamic profile of D-PAH are indistinguishable from other forms of PAH, its clinical course can be unpredictable and to some degree dependent on removal of the offending agent. Read More

    Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.
    Am J Physiol Lung Cell Mol Physiol 2018 May 1;314(5):L860-L870. Epub 2018 Feb 1.
    Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida , Tampa, Florida.
    Critically ill patients are commonly treated with high levels of oxygen, hyperoxia, for prolonged periods of time. Unfortunately, extended exposure to hyperoxia can exacerbate respiratory failure and lead to a high mortality rate. Mitochondrial A-kinase anchoring protein (Akap) has been shown to regulate mitochondrial function. Read More

    PLCγ1-PKCε-IPR1 signaling plays an important role in hypoxia-induced calcium response in pulmonary artery smooth muscle cells.
    Am J Physiol Lung Cell Mol Physiol 2018 May 1;314(5):L724-L735. Epub 2018 Feb 1.
    Department of Molecular and Cellular Physiology, Albany Medical College , Albany, New York.
    Hypoxia-induced pulmonary vasoconstriction (HPV) is attributed to an increase in intracellular Ca concentration ([Ca]) in pulmonary artery smooth muscle cells (PASMCs). We have reported that phospholipase C-γ1 (PLCγ1) plays a significant role in the hypoxia-induced increase in [Ca] in PASMCs and attendant HPV. In this study, we intended to determine molecular mechanisms for hypoxic Ca and contractile responses in PASMCs. Read More

    Emerging therapeutics in pulmonary hypertension.
    Am J Physiol Lung Cell Mol Physiol 2018 May 1;314(5):L769-L781. Epub 2018 Feb 1.
    Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh , Pittsburgh, Pennsylvania.
    Pulmonary hypertension (PH) is a progressive and often fatal illness presenting with nonspecific symptoms of dyspnea, lower extremity edema, and exercise intolerance. Pathologically, endothelial dysfunction leads to abnormal intimal and smooth muscle proliferation along with reduced apoptosis, resulting in increased pulmonary vascular resistance and elevated pulmonary pressures. PH is subdivided into five World Health Organization groups based on the disease pathology and specific cause. Read More

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