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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/28314804/stereological-monitoring-of-mouse-lung-alveolarization-from-the-early-post-natal-period-to-adulthood
#1
Agnieszka Pozarska, José Alberto Rodríguez-Castillo, David Emanuel Surate Solaligue, Aglaia Ntokou, Philipp Rath, Ivana Mižíková, Alicia Madurga, Konstantin Mayer, István Vadász, Susanne Herold, Katrin Ahlbrecht, Werner Seeger, Rory E Morty
Post-natal lung maturation generates a large number of small alveoli, with concomitant thinning of alveolar septal walls, generating a large gas exchange surface area but minimizing the distance traversed by the gases. This demand for a large and thin gas exchange surface area is not met in disorders of lung development, such as bronchopulmonary dysplasia (BPD), histopathologically characterized by fewer, larger alveoli; and thickened alveolar septal walls. Diseases such as BPD are often modeled in the laboratory mouse to better understand disease pathogenesis, or develop new interventional approaches...
March 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28314803/omega-3-polyunsaturated-fatty-acids-accelerate-airway-repair-by-activating-ffa4-in-club-cells
#2
Kyoung-Pil Lee, Soo-Jin Park, Saeromi Kang, Jung-Min Koh, Koichi Sato, Hae Young Chung, Fumikazu Okajima, Dong-Soon Im
A GPCR named FFA4 (also known as GPR120) was found to act as a GPCR for omega-3 polyunsaturated fatty acids. Its expression has been reported in lung epithelial club cells. The authors investigated whether supplementation of the omega-3 fatty acids benefits lung health. Omacor® (7.75 mg kg-1), clinically prescribed preparation of omega-3 fatty acids and FFA4-knockout mice were utilized in a naphthalene-induced mouse model of acute airway injury (one injection of 30 mg kg-1, i.p.). Naphthalene injection induced complete destruction of bronchiolar epithelial cells within a day...
March 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28314802/an-ex-vivo-model-to-induce-early-fibrosis-like-changes-in-human-precision-cut-lung-slices
#3
Hani N Alsafadi, Claudia A Staab-Weijnitz, Mareike Lehmann, Michael Lindner, Britta Peschel, Melanie Königshoff, Darcy Elizabeth Wagner
IPF is a devastating chronic interstitial lung disease (ILD) characterized by lung tissue scarring and high morbidity. Lung epithelial injury, myofibroblast activation, and deranged repair are believed to be key processes involved in disease onset and progression but the exact molecular mechanisms behind IPF remain unclear. Several drugs have been shown to slow disease progression, but treatments which halt or reverse IPF progression have not been identified. Ex vivo models of human lung have been proposed for drug discovery, one of which is precision-cut lung slices (PCLS)...
March 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283479/pkc-dependent-regulation-of-kv7-5-channels-by-the-bronchoconstrictor-histamine-in-human-airway-smooth-muscle-cells
#4
Jennifer M Haick, Lioubov I Brueggemann, Leanne L Cribbs, Mitchell F Denning, Jeffrey Schwartz, Kenneth L Byron
Kv7 potassium channels have recently been found to be expressed and functionally important for relaxation of airway smooth muscle. Previous research suggests that native Kv7 currents are inhibited following treatment of freshly isolated airway smooth muscle cells with bronchoconstrictor agonists, and in intact airways inhibition of Kv7 channels is sufficient to induce bronchiolar constriction. However, the mechanism by which Kv7 currents are inhibited by bronchoconstrictor agonists has yet to be elucidated...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283478/annexin-a2-contributes-to-lung-injury-and-fibrosis-by-augmenting-factor-xa-fibrogenic-activity
#5
Michael Schuliga, Jade Jaffar, Asres Berhan, Shenna Langenbach, Trudi Harris, David Waters, Peter Vee Sin Lee, Christopher Grainge, Glen Westall, Darryl Knight, Alastair G Stewart
In lung injury and disease, including idiopathic pulmonary fibrosis (IPF), extravascular factor X is converted into factor Xa (FXa), a coagulant protease with fibrogenic actions. Extracellular annexin A2 binds to FXa, augmenting activation of the protease activated receptor-1 (PAR-1). In this study, the contribution of annexin A2 in lung injury and fibrosis was investigated. Annexin A2 immunoreactivity was observed in regions of fibrosis, including associated with fibroblasts in lung tissue of IPF patients...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283477/lung-epithelial-cell-focal-adhesion-kinase-signaling-inhibits-lung-injury-and-fibrosis
#6
Amanda K Wheaton, Manisha Agarwal, Shijing Jia, Kevin K Kim
Progressive pulmonary fibrosis is a devastating consequence of many acute and chronic insults to the lung. Lung injury leads to alveolar epithelial cell (AEC) death, destruction of the basement membrane and activation of TGFβ. There is subsequent resolution of the injury and a coordinated and concurrent initiation of fibrosis. Both of these processes may involve activation of similar intracellular signaling pathways regulated in part by dynamic changes to the extracellular matrix. Matrix signaling can augment the pro-fibrotic fibroblast response to TGFβ...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283476/alveolar-non-selective-channels-are-asic1a-%C3%AE-enac-channels-and-contribute-to-afc
#7
Phi T Trac, Tiffany L Thai, Valerie Linck, Li Zou, Megan M Greenlee, Qiang Yue, Otor K Al-Khalili, Abdel A Alli, Amity F Eaton, Douglas C Eaton
A thin fluid layer in alveoli is normal and results from a balance of fluid entry and fluid uptake by transepithelial salt and water reabsorption. Conventional wisdom suggests the reabsorption is via epithelial Na(+) channels (ENaC), but if all Na(+) reabsorption was via ENaC, then amiloride, an ENaC inhibitor, should block AFC. But amiloride blocks only half of AFC. The reason for failure to block is clear from single channel measurements from alveolar epithelial cells: ENaC channels are observed, but another channel is present at the same frequency that is non-selective for Na(+) over K(+), has a larger conductance, and shorter open and closed times...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283475/rhinovirus-bacteria-co-exposure-synergistically-induces-ccl20-production-from-human-bronchial-epithelial-cells
#8
Barbara A Maciejewski, Kyla C Jamieson, Jason W Arnason, Cora Kooi, Shahina Wiehler, Suzanne L Traves, Richard Leigh, David Proud
Exacerbations of chronic obstructive pulmonary disease (COPD) are triggered by viral or bacterial pathogens, with human rhinovirus (HRV) and nontypeable Haemophilus influenzae (NTHI) among the most commonly detected pathogens. Patients who suffer from concomitant viral and bacterial infection have more severe exacerbations. The airway epithelial cell is the initial site of viral and bacterial interactions, and CCL20 is an epithelial chemokine that attracts immature dendritic cells to the airways, and can act as an antimicrobial...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283474/acid-sphingomyelinase-mediates-murine-acute-lung-injury-following-transfusion-of-aged-platelets
#9
Mark John McVey, Michael Kim, Arata Tabuchi, Victoria Srbely, Lukasz Japtok, Christoph Arenz, Ori Rotstein, Burkhard Kleuser, John Wesley Semple, Wolfgang Michael Kuebler
Pulmonary complications from stored blood products are the leading cause of mortality related to transfusion. Transfusion related acute lung injury is mediated by antibodies or bioactive mediators, yet, underlying mechanisms are incompletely understood. Sphingolipids such as ceramide regulate lung injury, and their composition changes as a function of time in stored blood. Here, we tested the hypothesis that aged platelets may induce lung injury via a sphingolipid-mediated mechanism. To assess this hypothesis, a two hit mouse model was devised...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283473/loss-of-lung-wwox-expression-causes-neutrophilic-inflammation
#10
Sunit Singla, Jiwang Chen, Shruthi Sethuraman, Justin R Sysol, Amulya Gampa, Shuangping Zhao, Roberto F Machado
The tumor suppressor, WWOX, exhibits regulatory interactions with an array of transcription factors and signaling molecules that are positioned at the well-known crossroads between inflammation and cancer. WWOX is also subject to downregulation by genotoxic environmental exposures, making it of potential interest to the study of lung pathobiology. Knockdown of lung WWOX expression in mice was observed to cause neutrophil influx, and accompanied by a corresponding vascular leak and inflammatory cytokine production...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28258108/newly-divided-eosinophils-limit-ozone-induced-airway-hyperreactivity-in-non-sensitized-guinea-pigs
#11
Sarah Anne Wicher, David B Jacoby, Allison D Fryer
Ozone causes vagally-mediated airway hyperreactivity and recruits inflammatory cells, including eosinophils, to lungs where they mediate ozone-induced hyperreactivity one day after exposure, but are paradoxically protective three days later. To test the role of newly divided eosinophils in ozone-induced airway hyperreactivity in sensitized and non-sensitized guinea pigs. Non-sensitized and sensitized guinea pigs were treated with 5-bromo-2-deoxyuridine (BrdU) to label newly divided cells and were exposed to air or ozone for 4 hours...
March 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28258107/non-antibiotic-macrolides-restore-airway-macrophage-phagocytic-function-with-potential-anti-inflammatory-effects-in-chronic-lung-diseases
#12
Sandra J Hodge, Hai Tran, Rhys Hamon, Eugene Roscioli, Greg Hodge, Hubertus Jersmann, Miranda Ween, Paul N Reynolds, Arthur Yeung, Jennifer Treiberg, Sibylle Wilbert
We reported defective efferocytosis associated with cigarette smoking and/or airway inflammation in chronic lung diseases including COPD, severe asthma and childhood bronchiectasis. We also showed defects in phagocytosis of non-typeable H. influenzae (NTHi), a common colonizer of the lower airway in these diseases. These defects could be substantially overcome with low-dose Azithromycin; however, chronic usage may induce bacterial resistance. We investigated two novel macrolides, GS-459755 (2'-desoxy-9-(S)-erythromycylamine) and GS-560660 (Azithromycin-based 2'-desoxy molecule) with significantly diminished antibiotic activity against S...
March 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28258106/profiling-of-ards-pulmonary-edema-fluid-identifies-a-metabolically-distinct-subset
#13
Angela J Rogers, Kevin Contrepois, Manhong Wu, Ming Zheng, Gary Peltz, Lorraine B Ware, Michael A Matthay
There is considerable biologic and physiologic heterogeneity among patients who meet standard clinical criteria for acute respiratory distress syndrome (ARDS). In this study, we tested the hypothesis that there exists a sub-group of ARDS patients who exhibit a metabolically distinct profile. We examined undiluted pulmonary edema fluid obtained at the time of endotracheal intubation from 16 clinically phenotyped ARDS patients and 13 control patients with hydrostatic pulmonary edema. Non-targeted metabolic profiling was carried out on the undiluted edema fluid...
March 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28258105/effect-of-%C3%AE-7-nicotinic-acetylcholine-receptor-activation-on-cardiac-fibroblasts-a-mechanism-underlying-rv-fibrosis-associated-with-cigarette-smoke-exposure
#14
Alexander Vang, Richard T Clements, Havovi Chichger, Nouaying Kue, Ayed Allawzi, Kelly A O'Connell, Euy-Myoung Jeong, Samuel Dudley, Pavlo Sakhatskyy, Qing Lu, Peng Zhang, Sharon Rounds, Gaurav Choudhary
INTRODUCTION: Right ventricular dysfunction is associated with numerous smoking-related illnesses including chronic obstructive pulmonary disease (COPD) where it is present even in absence of pulmonary hypertension. It is unknown if exposure to cigarette smoke has direct effects on RV function and cardiac fibroblast proliferation or collagen synthesis. In this study, we evaluated cardiac function and fibrosis in mice exposed to cigarette smoke (CS) and determined mechanisms of smoke-induced changes in cardiac fibroblast signaling and fibrosis...
March 3, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28235951/human-airway-trypsin-like-protease-a-serine-protease-involved-in-respiratory-diseases
#15
Awen Menou, JanWillem Duitman, Pauline Flajolet, Jean-Michel Sallenave, Arnaud A Mailleux, Bruno Crestani
More than 2% of all human genes are coding for a complex system of more than 700 proteases and protease inhibitors. Amongst them, serine proteases play extraordinary diverse functions in different physiological and pathological processes. The Human Airway Trypsin-like protease (HAT), also referred to as TMPRSS11D and serine 11D, belongs to the emerging family of cell surface proteolytic enzymes, the type II transmembrane serine proteases (TTSPs). Through the cleavage of its four major identified substrates, HAT triggers specific responses, notably in epithelial cells, within the pericellular and extracellular environment, including notably inflammatory cytokine production, inflammatory cell recruitment or anticoagulant processes...
February 24, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28235950/the-mast-cell-b-cell-axis-in-lung-vascular-remodeling-and-pulmonary-hypertension
#16
Siegfried Breitling, Zhang Hui, Diana Zabini, Yijie Hu, Julia Hoffmann, Neil M Goldenberg, Arata Tabuchi, Roland Buelow, Claudia Dos Santos, Wolfgang Michael Kuebler
Over the past years, a critical role for the immune system and in particular, for mast cells, in the pathogenesis of pulmonary hypertension (PH) has emerged. However, the way in which mast cells promote PH is still poorly understood. Here, we investigated the mechanisms by which mast cells may contribute to PH, specifically focusing on the interaction between the innate and adaptive immune response and the role of B-cells and autoimmunity. Experiments were performed in Sprague Dawley rats and B-cell deficient JH-KO rats in the monocrotaline, sugen-hypoxia and the aortic banding model of PH...
February 24, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28235949/bmp4-inhibits-pdgf-induced-proliferation-and-collagen-synthesis-via-pka-mediated-inhibition-of-calpain-2-in-pulmonary-artery-smooth-muscle-cells
#17
PengCheng Cai, Laszlo Kovacs, Sam Dong, Guangyu Wu, Yunchao Su
In the present study, we investigated the effect of bone morphogenetic protein 4 (BMP4) on PDGF-induced proliferation and collagen synthesis in PASMCs. Normal human PASMCs were incubated with and without PDGF-BB in the absence and presence of BMP4 for 0.5 to 24 h. Then the protein levels of collagen-I, p-Smad2/3, p-Smad1/5, and intracellular active TGFβ1, calpain activity and cell proliferation were measured. The results showed that BMP4 induced an increase in p-Smad1/5 but had no effect on the protein levels of collagen-I, p-Smad2/3, and intracellular active TGFβ1, and calpain activity in PASMCs...
February 24, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213473/central-role-of-t-helper-17-cells-in-chronic-hypoxia-induced-pulmonary-hypertension
#18
Levi D Maston, David T Jones, Wieslawa Giermakowska, Tamara A Howard, Judy L Cannon, Wei Wang, Yongyi Wei, Weimin Xuan, Thomas C Resta, Laura V Gonzalez Bosc
RATIONALE: Inflammation is a prominent pathologic feature in pulmonary arterial hypertension as demonstrated by pulmonary vascular infiltration of inflammatory cells, including T and B lymphocytes. However, the contribution of the adaptive immune system is not well characterized in pulmonary hypertension caused by chronic hypoxia. CD4(+) T cells are required for initiating and maintaining inflammation, suggesting these cells could play an important role in the pathogenesis of hypoxic pulmonary hypertension...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213472/%C3%AE-2-microglobulin-participates-in-development-of-lung-emphysema-by-inducing-lung-epithelial-cells-senescence
#19
Na Gao, Ying Wang, Chun-Ming Zheng, Yan-Li Gao, Hui Li, Yan Li, Ting-Ting Fu, Li-Li Xu, Wei Wang, Sun Ying, Kewu Huang
β2-microglobulin (β2m), the light chain of major histocompatibility complex class 1 (MHC I), has been identified as a pro-aging factors and involved in the pathogenesis of neurodegenerative disorders by driving cognitive and regenerative impairments. However, little attention has focused on the effect of β2m in development of lung emphysema. Here, we found that concentrations of β2m in plasma were significantly elevated in patients with lung emphysema than those in normal control subjects (1.89 ± 0.12 mg/l vs 1...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28213471/attenuation-of-endoplasmic-reticulum-stress-by-caffeine-ameliorates-hyperoxia-induced-lung-injury
#20
Ru-Jeng Teng, Xigang Jing, Teresa Michalkiewicz, Adeleye J Afolayan, Tzong-Jin Wu, Girija G Konduri
Rodent pups exposed to hyperoxia develop lung changes similar to bronchopulmonary dysplasia (BPD) in extremely premature infants. Oxidative stress from hyperoxia can injure developing lungs through endoplasmic reticulum (ER) stress. Early caffeine treatment decreases the rate of BPD, but the mechanisms remain unclear. We hypothesized that caffeine attenuates hyperoxia-induced lung injury through its chemical chaperone property. Sprague-Dawley rat pups were raised either in 90% (hyperoxia) or 21% (normoxia) oxygen from postnatal day 1 (P1) to postnatal day 10 (P10) and then recovered in 21% oxygen until P21...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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