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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/28428175/flavored-e-cigarette-liquids-reduce-proliferation-and-viability-in-the-calu3-airway-epithelial-cell-line
#1
Temperance R Rowell, Steven L Reeber, Shernita L Lee, Rachel A Harris, Rachel C Nethery, Amy H Herring, Gary L Glish, Robert Tarran
E-cigarettes are generally thought of as a safer smoking alternative to traditional cigarettes. However, little is known about the effects of e-cigarette liquids (e-liquids) on the lung. Since over 7,000 unique flavors have been identified for purchase in the USA, our goal was to conduct a screen that would test whether different flavored e-liquids exhibited different toxicant profiles. We tested the effects of 13 different flavored e-liquids (with nicotine and propylene glycol/vegetable glycerin (PG/VG) serving as controls) on a lung epithelial cell line (CALU3)...
April 20, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28428174/klotho-an-anti-aging-molecule-attenuates-oxidant-induced-alveolar-epithelial-cell-mtdna-damage-and-apoptosis
#2
Seok-Jo Kim, Paul Cheresh, Mesut Eren, Renea P Jablonski, Anjana Yeldandi, Karen M Ridge, Gr Scott Budinger, Dong-Hyun Kim, Myles S Wolf, Douglas Vaughan, David W Kamp
Alveolar epithelial cell (AEC) apoptosis and inadequate repair resulting from 'exaggerated' lung aging and mitochondrial dysfunction are critical determinants promoting lung fibrosis. α-Klotho, which is an anti-aging molecule that is expressed predominantly in the kidney and secreted in the blood, can protect lung epithelial cells against hyperoxia-induced apoptosis. We reasoned that Klotho protects AEC exposed to oxidative stress in part by maintaining mitochondrial DNA (mtDNA) integrity and mitigating apoptosis...
April 20, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28408366/acute-brain-trauma-lung-injury-and-pneumonia-more-than-just-altered-mental-status-and-decreased-airway-protection
#3
Parker J Hu, Jean-Francois Pittet, Jeffrey D Kerby, Patrick L Bosarge, Brant M Wagener
Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Even when patients survive the initial insult, there is significant morbidity and mortality secondary to subsequent pulmonary edema, acute lung injury and nosocomial pneumonia. While the relationship between TBI and secondary pulmonary complications is recognized, little is known about the mechanistic interplay of the two phenomena. Changes in mental status secondary to acute brain injury certainly impair airway- and lung-protective mechanisms...
April 13, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28408365/immunomodulators-targeting-marco-expression-improve-resistance-to-post-influenza-bacterial-pneumonia
#4
Muzo Wu, John G Gibbons, Glen M Deloid, Alice S Bedugnis, Rajesh K Thimmulappa, Shyam Biswal, Lester Kobzik
Down-regulation of the alveolar macrophage (AM) macrophage receptor with collagenous structure (MARCO) leads to susceptibility to post-influenza bacterial pneumonia, a major cause of morbidity and mortality. We sought to determine whether immunomodulation of MARCO could improve host defense and resistance to secondary bacterial pneumonia. RNAseq analysis identified a striking increase of MARCO expression between days 9 and 11 after influenza infection and indicated important roles for Akt and Nrf2 in MARCO recovery...
April 13, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385814/tnf%C3%AE-enhances-force-generation-in-airway-smooth-muscle
#5
Murat Dogan, Young-Soo Han, Philippe F Delmotte, Gary C Sieck
Airway inflammation is a hallmark of asthma triggering airway smooth muscle (ASM) hyperreactivity and airway remodeling. TNFα increases both agonist-induced cytosolic Ca(2+) concentration and force in ASM. The effects of TNFα on ASM force may also be due to an increase in Ca(2+) sensitivity, cytoskeletal remodeling and/or changes in contractile protein content. We hypothesized that 24-h exposure TNFα increases ASM force by changing actin and myosin heavy chain (MyHC) content and/or polymerization. Porcine ASM strips were permeabilized with 10% Triton X-100, and force was measured in response to increasing concentrations of Ca(2+) (pCa 9...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385813/acidosis-increases-the-susceptibility-of-respiratory-epithelial-cells-to-pseudomonas-aeruginosa-induced-cytotoxicity
#6
Iviana M Torres, Sally Demirdjian, Jennifer Vargas, Britton C Goodale, Brent L Berwin
Bacterial infection can lead to acidosis of the local microenvironment. While this is believed to exacerbate disease pathogenesis, the mechanisms by which changes in pH alter disease progression are poorly understood. In this report we test the hypothesis that acidosis enhances respiratory epithelial cell death in response to infection with Pseudomonas aeruginosa. Our findings support that acidosis in the context of P. aeruginosa infection results in increased epithelial cell cytotoxicity due to ExoU intoxication...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385812/sirtuin-7-is-decreased-in-pulmonary-fibrosis-and-regulates-the-fibrotic-phenotype-of-lung-fibroblasts
#7
Anne Elizabeth Wyman, Zahid Noor, Rita Fishelevich, Virginia Lockatell, Nirav G Shah, Nevins W Todd, Sergei P Atamas
Pulmonary fibrosis is a severe condition with no cure and limited therapeutic options. Better understanding of its pathophysiology is needed. Recent studies have suggested that pulmonary fibrosis may be driven by accelerated aging-related mechanisms. Sirtuins (SIRTs), particularly SIRT1, -3, and -6, are well-known mediators of aging, however limited data exist on the contribution of sirtuins to lung fibrosis. We assessed the mRNA and protein levels of all seven known sirtuins in primary lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD) in comparison with lung fibroblasts from healthy controls...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385811/modified-mesenchymal-stem-cells-using-mirna-transduction-alter-lung-injury-in-a-bleomycin-model
#8
Luai Huleihel, Jacobo Sellares, Nayra Cardenes, Diana Alvarez, Rosa Faner, Koji Sakamoto, Guoying Yu, Maria G Kapetanaki, Naftali Kaminski, Mauricio Rojas
Although different preclinical models have demonstrated a favorable role for bone marrow derived mesenchymal stem cells (B-MSC) in preventing fibrosis, this protective effect is not observed with late administration of these cells, when fibrotic changes are consolidated. We sought to investigate whether the late administration of B-MSCs overexpressing microRNAs (miRNAs) let-7d (anti-fibrotic) or miR-154 (pro-fibrotic) could alter lung fibrosis in a murine bleomycin model. Using lentiviral vectors we transduced miRNAs (let-7d or miR-154) or a control sequence into human B-MSCs...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385810/regulation-of-p53-mediated-changes-in-the-upa-fibrinolytic-system-and-in-lung-injury-by-loss-of-surfactant-protein-c-expression-in-alveolar-epithelial-cells
#9
Bijesh Puthusseri, Amarnath S Marudamuthu, Nivedita Tiwari, Jian Fu, Steven Idell, Sreerama Shetty
Pulmonary surfactant protein-C (SP-C) expression by type II alveolar epithelial cells (AECs) is markedly reduced in diverse types of lung injuries and is often associated with AEC apoptosis. It is unclear whether loss of SP-C contributes to the increased p53 and urokinase-type plasminogen activator (uPA) system cross talk and apoptosis of AECs. We therefore inhibited SP-C expression in human and murine AECs using lentivirus vector expressing shRNA and tested p53 and downstream changes in uPA-fibrinolytic system...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385809/free-actin-impairs-macrophage-bacterial-defenses-via-scavenger-receptor-marco-interaction-with-reversal-by-plasma-gelsolin
#10
Christine M Ordija, Terry Ting-Yu Chiou, Zhiping Yang, Glen M Deloid, Melina de Oliveira Valdo, Zhi Wang, Alice Bedugnis, Terry L Noah, Samuel Jones, Henry Koziel, Lester Kobzik
Lung injury can release intracellular actin into the alveolar milieu, and is also associated with increased susceptibility to secondary infections. We investigated the effect of free (extracellular) actin on lung macrophage host defense functions. Western blot analysis demonstrated free actin release into the lung lavage fluids of mouse models of ozone injury, influenza infection and secondary pneumococcal pneumonia, and in samples from patients following burn and inhalation injury. Using levels comparable to those observed in lung injury, we found that free actin markedly inhibited murine lung macrophage binding and uptake in vitro of S...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385808/does-lack-of-glutathione-peroxidase-1-gene-expression-exacerbate-lung-injury-induced-by-neonatal-hyperoxia-in-mice
#11
Sheena Bouch, Megan O'Reilly, Judy B de Haan, Richard Harding, Foula Sozo
Supplemental oxygen (O2) increases the risk of lung injury in preterm infants owing to an immature antioxidant system. Our objective was to determine whether impairing antioxidant defense by decreasing glutathione peroxidase 1 (GPx1) gene expression increases the injurious effects of hyperoxia. GPx1(+/+) and GPx1(-/-) C57Bl/6J mice were exposed to 21% O2 (Air) or 40% O2 (Hyperoxia; Hyp) from birth to postnatal day 7 (P7d); they were killed at P7d or maintained in air until adulthood (P56d) to assess short-term and long-term effects, respectively...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28385807/pyk2-phosphorylation-of-ve-ptp-downstream-of-stim1-induced-ca2-entry-regulates-disassembly-of-adherens-junctions
#12
Dheeraj Soni, Sushil C Regmi, Dong-Mei Wang, Auditi DebRoy, You-Yang Zhao, Stephen M Vogel, Asrar B Malik, Chinnaswamy Tiruppathi
VE-PTP stabilizes endothelial adherens junctions (AJs) through constitutive dephosphorylation of VE-cadherin. Here we investigated the role of STIM1 activation of store-operated Ca2+ entry (SOCE) in regulating adherens junction assembly. We observed that SOCE induced by STIM1 activated Pyk2 in human lung microvascular endothelial cells (ECs) and induced tyrosine phosphorylation of VE-PTP at Y1981. Pyk2-induced tyrosine phosphorylation of VE-PTP promoted Src binding to VE-PTP, Src activation, and subsequent VE-cadherin phosphorylation, and thereby increased the endothelial permeability response...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360114/ror%C3%AE-dependent-type-2-innate-lymphoid-cells-are-required-and-sufficient-for-mucous-metaplasia-in-immature-mice
#13
Charu Rajput, Tracy X Cui, Mingyuan Han, Jing Lei, Joanna L Hinde, Qian Wu, J Kelley Bentley, Marc B Hershenson
Early-life wheezing associated respiratory tract infection by rhinovirus (RV) is considered a risk factor for asthma development. We have shown that RV infection of 6 day-old BALB/c mice, but not mature mice, induces an asthma-like phenotype which is associated with an increase in the population of type 2 innate lymphoid cells (ILC2s) and dependent on IL-13 and IL-25. We hypothesize that ILC2s are required and sufficient for development of the asthma-like phenotype in immature mice. Mice were infected with RV1B on day 6 of life and treated with vehicle or a chemical inhibitor of retinoic acid receptor-related orphan receptor (ROR)-α, SR3335 (15 mg/kg/day intraperitoneally for 7 days)...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360113/directional-preference-of-airway-smooth-muscle-mass-increase-in-human-asthmatic-airways
#14
Gijs Ijpma, Alice Panariti, Anne-Marie Lauzon, James G Martin
Airway smooth muscle (ASM) orientation and morphology determine the ability of the muscle to constrict the airway. In asthma, ASM mass is increased, but it is unknown whether ASM orientation and morphology are altered as well, or whether the remodelling at the source of the mass increase is ongoing. We dissected human airway trees from asthmatic and control lungs. Stained, intact airway sections were imaged in axial projection to show ASM bundle orientation, while cross-sectional histological slides were used to assess ASM area, bundle thickness and ASM bundle to basement membrane distance...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360112/apoptotic-cell-death-in-rat-lung-following-mustard-gas-inhalation
#15
Devon Katherine Andres, Brian M Keyser, Ashley A Melber, Betty Jean Benton, Tracey A Hamilton, Denise M Kniffin, Magaret E Martens, Radharaman Ray
To investigate apoptosis as a mechanism of sulfur mustard (SM) inhalation injury in animals, we studied different caspases (caspase-8, -9, -3 and -6) in the lungs from a ventilated rat SM aerosol inhalation model. SM activated all four caspases in cells obtained from bronchoalveolar lavage fluid (BALF) as early as 6 hr after exposure. Caspase-8, which is known to initiate the extrinsic Fas-mediated pathway of apoptosis, was increased 5-fold between 6 to 24 hr, decreasing to the unexposed-control level at 48 hr...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360111/the-effects-of-electronic-cigarette-aerosol-exposure-on-inflammation-and-lung-function-in-mice
#16
Alexander N Larcombe, Maxine A Janka, Benjamin J Mullins, Luke J Berry, Arne Bredin, Peter J Franklin
Electronic cigarette usage is increasing worldwide, yet there is a paucity of information on the respiratory health effects of electronic cigarette aerosol exposure. This study aimed to assess whether exposure to electronic-cigarette (e-cigarette) aerosol would alter lung function and pulmonary inflammation in mice, and to compare the severity of any alterations with mice exposed to mainstream tobacco smoke. Female BALB/c mice were exposed for 8 weeks to tobacco smoke, medical air (control) or one of 4 different types of e-cigarette aerosol...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360110/the-cftr-trafficking-mutation-f508del-inhibits-the-constitutive-activity-of-slc26a9
#17
Carol A Bertrand, Shalini Mitra, Sanjay K Mishra, Xiaohui Wang, Yu Zhao, Joseph M Pilewski, Dean R Madden, Raymond A Frizzell
Several members of the SLC26A family of anion transporters associate with CFTR, forming complexes in which CFTR and SLC26A functions are reciprocally regulated. This association is thought to be facilitated by PDZ scaffolding interactions. CFTR has been shown to be positively regulated by NHERF-1, and negatively regulated by CAL in airway epithelia. However, it's unclear which PDZ-domain protein(s) interact with SLC26A9, a SLC26A family member found in airway epithelia. We have previously shown that primary, human bronchial epithelia (HBE) from non-CF donors exhibit constitutive anion secretion attributable to SLC26A9...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28360109/focal-adhesion-kinase-signaling-determines-the-fate-of-lung-epithelial-cells-in-response-to-tgf-%C3%AE
#18
Qiang Ding, Indhu Subramanian, Tracy R Luckhardt, Pulin Che, Meghna Waghray, Xueke Zhao, Nathaniel Bone, Ashish R Kurundkar, Louise Hecker, Meng Hu, Yong Zhou, Jeffrey Craig Horowitz, Ragini Vittal, Victor J Thannickal
Alveolar epithelial cell (AEC) injury and apoptosis are prominent pathological features of idiopathic pulmonary fibrosis (IPF). There is evidence of AEC plasticity in lung injury repair responses and in IPF. In this report, we explore the role of focal adhesion kinase (FAK) signaling in determining the fate of lung epithelial cells in response to TGF-β1. Rat type II alveolar epithelial cells (RLE-6TN) were treated with or without TGF-β1, and the expression of mesenchymal phenotype and function were analyzed...
March 30, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28336814/airway-smooth-muscle-dysfunction-in-pompe-gaa-mice
#19
Allison M Keeler, Donghai Liu, Marina Zieger, Lang Xiong, Jeffrey Salemi, Karl Bellve, Barry J Byrne, David D Fuller, Ronghua ZhuGe, Mai K ElMallah
Pompe disease is an autosomal recessive disorder caused by a deficiency of acid alpha-glucosidase (GAA) - an enzyme responsible for hydrolyzing lysosomal glycogen. Deficiency of GAA leads to systemic glycogen accumulation in the lysosomes of skeletal muscle, motor neurons and smooth muscle. Skeletal muscle and motor neuron pathology are known to contribute to respiratory insufficiency in Pompe disease, but the role of airway pathology has not been evaluated. Here we propose that GAA enzyme deficiency disrupts the function of the trachea and bronchi, and this lower airway pathology contributes to respiratory insufficiency in Pompe disease...
March 23, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28336813/the-innate-immune-response-in-fetal-lung-mesenchymal-cells-targets-vegfr2-expression-and-activity
#20
Rachel M Medal, Amanda M Im, Yasutoshi Yamamoto, Omar Lakhdari, Timothy S Blackwell, Hal M Hoffman, Debashis Sahoo, Lawrence S Prince
In preterm infants, soluble inflammatory mediators target lung mesenchymal cells, disrupting airway and alveolar morphogenesis. However, how mesenchymal cells respond directly to microbial stimuli remains poorly characterized. Our objective was to measure the genome-wide innate immune response in fetal lung mesenchymal cells exposed to the bacterial endotoxin lipopolysaccharide (LPS). Using Affymetrix MoGene 1.0st arrays, we showed that LPS induced expression of unique innate immune transcripts heavily weighted toward CC and CXC family chemokines...
March 23, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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