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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/30024307/human-pulmonary-endothelial-cell-permeability-after-exposure-to-lps-stimulated-leukocyte-supernatants-derived-from-patients-with-early-sepsis
#1
Aleksandra Leligdowicz, Lauren F Chun, Alejandra Jauregui, Kathryn Vessel, Kathleen D Liu, Carolyn S Calfee, Michael A Matthay
Systemic immune activation is the hallmark of sepsis, which can result in endothelial injury and the Acute Respiratory Distress Syndrome (ARDS). The aim of this study was to investigate heterogeneity in sepsis-mediated endothelial permeability using primary human pulmonary microvascular endothelial cells (HPMECs) and the Electric Cell-substrate Impedance Sensing (ECIS) platform. After plasma removal, cellular component of whole blood from 35 ICU patients with early sepsis was diluted with media and stimulated with either LPS or control media...
July 19, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/30024306/ischemia-reperfusion-induces-death-receptor-independent-necroptosis-via-calpain-stat3-activation-in-a-lung-transplant-setting
#2
Hyunhee Kim, Ricardo Zamel, Xiao-Hui Bai, Christina Lu, Sara Keshavjee, Shaf Keshavjee, Mingyao Liu
Ischemia-reperfusion (IR)-induced lung injury undermines lung transplantation (LTx) outcomes by predisposing lung grafts to primary graft dysfunction (PGD). Necrosis is a feature of IR-lung injury. However, regulated-necrosis (RN) with specific signaling pathways has not been explored in LTx setting. In this study, we investigated the role of RN in IR-induced lung injury. To study IR-induced cell-death, we simulated LTx procedure using our cell culture model with human lung epithelial (BEAS-2B) cells. After 18 h of cold ischemic time (CIT) followed by reperfusion, caspase-independent cell-death, mitochondrial-ROS production and mitochondrial-membrane permeability were significantly increased...
July 19, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/30024305/the-thioredoxin-reductase-inhibitor-auranofin-induces-heme-oxygenase-1-in-lung-epithelial-cells-via-nrf2-dependent-mechanisms
#3
Katelyn Dunigan, Qian Li, Rui Li, Morgan L Locy, Stephanie B Wall, Trent E Tipple
Thioredoxin reductase-1 (TXNRD1) inhibition effectively activates nuclear factor (erythroid-derived 2)-like 2 (Nrf2) responses and attenuates lung injury in acute respiratory distress syndrome (ARDS) and bronchopulmonary dysplasia (BPD) models. Upon TXNRD1 inhibition, heme oxygenase-1 (HO-1) is disproportionally increased compared with Nrf2 target NADPH quinone oxidoreductase-1 (NQO1). HO-1 has been investigated as a potential therapeutic target in both ARDS and BPD. TXNRD1 is predominantly expressed in airway epithelial cells; however, the mechanism of HO-1 induction by TXNRD1 inhibitors is unknown...
July 19, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/30024304/microrna-dysregulation-in-lung-injury-the-role-of-the-mir-26a-epha2-axis-in-regulation-of-endothelial-permeability
#4
Ryan J Good, Laura Hernandez-Lagunas, Ayed Allawzi, Joanne K Maltzahn, Christine U Vohwinkel, Arun K Upadhyay, Uday Kompella, Konstantin G Birukov, Todd C Carpenter, Carmen C Sucharov, Eva Nozik-Grayck
MicroRNAs (miRNAs) are non-coding RNAs that regulate gene expression in many diseases, though the contribution of miRNAs to the pathophysiology of lung injury remains obscure. We hypothesized that dysregulation of miRNA expression drives the changes in key genes implicated in the development of lung injury. To test our hypothesis, we utilized a model of lung injury induced early after administration of intratracheal bleomycin (0.1 U). Wild-type mice were treated with bleomycin or PBS and lungs were collected at 4 or 7 days...
July 19, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29999407/sphingosine-1-phosphate-induces-airway-smooth-muscle-cells-proliferation-migration-and-contraction-by-modulating-hippo-signaling-effector-yap
#5
Lu Liu, Cui Zhai, Yilin Pan, Yanting Zhu, Wenhua Shi, Jian Wang, Xin Yan, Xiaofan Su, Yang Song, Li Gao, Manxiang Li
Sphingosine-1-phosphate (S1P), a bioactive lipid, has been shown to be elevated in the airways of individuals with asthma and modulates the airway smooth muscle cells (ASMCs) functions, yet its underlying molecular mechanisms are not completely understood. The aim of the present study is to address this issue. S1P induced yes-associated protein (YAP) de-phosphorylation and nuclear localization via S1PR2/3/Rho-associated protein kinase (ROCK) pathway, and this in turn increased forkhead box M1 (FOXM1) and cyclin D1 expression leading to ASMCs proliferation, migration and contraction...
July 12, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29975104/twisted-hif-re-visiting-smooth-muscle-hif-1%C3%AE-signaling-in-pulmonary-hypertension
#6
Yuanjun Steven Shen, Elena A Goncharova
No abstract text is available yet for this article.
July 5, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29975103/dissociation-cellular-isolation-and-initial-molecular-characterization-of-neonatal-and-pediatric-human-lung-tissues
#7
Gautam Bandyopadhyay, Heidie L Huyck, Ravi S Misra, Soumyaroop Bhattacharya, Qian Wang, Jared Mereness, Jacquelyn A Lillis, Jason R Myers, John Ashton, Timothy Bushnell, Matthew Cochran, Jeanne Holden-Wiltse, Philip Katzman, Gail H Deutsch, Jeffrey A Whitsett, Yan Xu, Thomas Jay Mariani, Gloria S Pryhuber
Human lung morphogenesis begins by embryonic life and continues after birth into early childhood to form a complex organ with numerous morphologically and functionally distinct cell types. Pulmonary organogenesis involves dynamic changes in cell proliferation, differentiation, and migration of specialized cells derived from diverse embryonic lineages. Studying the molecular and cellular processes underlying formation of the fully functional lung requires isolating distinct pulmonary cell populations during development...
July 5, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29975102/lung-eosinophilia-induced-by-house-dust-mites-or-ovalbumin-is-modulated-by-nicotinic-receptor-alpha-7-and-inhibited-by-cigarette-smoke
#8
Lorise C Gahring, Elizabeth J Myers, Diane M Dunn, Robert B Weiss, Scott Warren Rogers
Eosinophilia (EOS) is an important component of airway inflammation and hyper-responsiveness in allergic reactions including those leading to asthma. While cigarette smoking (CS) is a significant contributor to long-term adverse outcomes in these lung disorders, there are also the curious reports of its ability to produce acute suppression of inflammatory responses including eosinophilia through poorly understood mechanisms. One possibility is that pro-inflammatory processes are suppressed by nicotine in CS acting through the nicotinic receptor α7 (α7)...
July 5, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29952222/evolution-of-ards-biomarkers-will-metabolomics-be-the-answer
#9
Sayed Metwaly, Andreanne Cote, Sarah J Donnelly, Mohammad M Banoei, Ahmed I Mourad, Brent W Winston
To date there is no clinically agreed upon diagnostic test for acute respiratory distress syndrome (ARDS): the condition is still diagnosed based on a constellation of clinical findings, laboratory tests and radiological images. Development of ARDS biomarkers has been in a state of continuous flux during the past four decades. To address ARDS heterogeneity, several studies have recently focused on subphenotying the disease based on observable clinical characteristics and associated blood biomarkers. However, the strong correlation between identified biomarkers and ARDS subphenotypes has yet to establish etiology hence the need for the adoption of other methodologies for studying ARDS...
June 28, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29952221/iloprost-attenuates-hyperoxia-mediated-impairment-of-lung-development-in-newborn-mice
#10
Nelida Olave, Charitharth Vivek Lal, Brian Halloran, Vineet Bhandari, Namasivayam Ambalavanan
Cyclooxygenase-2 (COX-2/PTGS2) mediates hyperoxia-induced impairment of lung development in newborn animals, and is increased in lungs of human infants with bronchopulmonary dysplasia (BPD). COX-2 catalyzes production of cytoprotective prostaglandins such as prostacyclin (PGI2) as well as pro-inflammatory mediators such as thromboxane A2 (TxA2). Our objective was to determine whether iloprost, a synthetic analog of prostacyclin, would attenuate hyperoxia effects in the newborn mouse lung. To test this hypothesis, newborn C57BL/6 mice along with their dams were exposed to normoxia (21%) or hyperoxia (85% O2) from 4 to 14 days of age in combination with daily i...
June 28, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29952220/mechanisms-of-organophosphorus-pesticide-toxicity-in-the-context-of-airway-hyperreactivity-and-asthma
#11
Frances C Shaffo, Ana Cristina Grodzki, Allison D Fryer, Pamela J Lein
Numerous epidemiologic studies have identified an association between occupational exposures to organophosphorus pesticides (OPs) and asthma or asthmatic symptoms in adults. Emerging epidemiologic data suggest that environmentally relevant levels of OPs may also be linked to respiratory dysfunction in the general population, and that in utero and/or early life exposures to environmental OPs may increase risk for childhood asthma. In support of a causal link between OPs and asthma, experimental evidence demonstrates that occupationally and environmentally relevant OP exposures induce bronchospasm and airway hyperreactivity in preclinical models...
June 28, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29952219/inhibition-of-lncrna-pfrl-prevents-pulmonary-fibrosis-by-disrupting-the-mir-26a-smad2-loop
#12
Hua Jiang, Yingzhun Chen, Tong Yu, Xiaoguang Zhao, Huitong Shan, Jian Sun, Lu Zhang, Xuelian Li, Hongli Shan, Haihai Liang
Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease with increasing mortality and poor prognosis. The current understanding of the role of long non-coding RNAs (lncRNAs) in IPF remain limited. In the present study, we identified a lncRNA NONMMUT022554, designated pulmonary fibrosis-regulatory lncRNA (PFRL), with unknown functions and found that its levels were increased in fibrotic lung tissues of mice and pulmonary fibroblasts exposed to TGF-β1. Furthermore, we found that enforced expression of PFRL induced fibroblast activation and collagen deposition, which could be mitigated by the overexpression of miR-26a...
June 28, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29952218/cell-surface-phenotyping-identifies-cd36-and-cd97-as-novel-markers-of-fibroblast-quiescence-in-lung-fibrosis
#13
Katharina Heinzelmann, Mareike Lehmann, Michael Gerckens, Nina Noskovičová, Marion Frankenberger, Michael Lindner, Rudolf Hatz, Jürgen Behr, Anne Hilgendorff, Melanie Königshoff, Oliver Eickelberg
Fibroblasts play an important role in lung homeostasis and disease. In lung fibrosis, fibroblasts adopt a proliferative and migratory phenotype, with increased expression of α-smooth muscle actin (αSMA) and enhanced secretion of extracellular matrix components. Comprehensive profiling of fibroblast heterogeneity is limited, due to a lack of specific cell-surface markers. We have previously profiled the surface proteome of primary human lung fibroblasts. Here, we sought to define and quantify a panel of cluster of differentiation markers in primary human lung fibroblasts and IPF lung tissue, using immunofluorescence and FACS analysis...
June 28, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29877097/a-pro-con-debate-current-controversies-in-pah-pathogenesis-at-the-american-thoracic-society-international-meeting-in-2017
#14
Wolfgang Michael Kuebler, Mark R Nicolls, Andrea Olschewski, Kohtaro Abe, Marlene Rabinovitch, Duncan J Stewart, Stephen Y Chan, Nicholas W Morrell, Stephen L Archer, Edda Spiekerkoetter
The following review summarizes the pro-con debate about current controversies regarding the pathogenesis of pulmonary arterial hypertension (PAH) that took place at the American Thoracic Society Conference in May 2017. Leaders in the field of PAH research discussed the importance of the immune system, the role of hemodynamic stress and endothelial apoptosis as well as bone morphogenetic protein receptor 2 (BMPR2) signaling in PAH pathogenesis. While this summary does not intend to resolve obvious conflicts in opinion, we hope that the presented arguments entice further discussions and draw a new generation of enthusiastic researchers into this vibrant field of science to bridge existing gaps for a better understanding and therapy of this fatal disease...
June 7, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29877096/subacute-tgf%C3%AE-expression-drives-inflammation-goblet-cell-hyperplasia-and-pulmonary-function-abnormalities-in-mice-with-effects-dependent-on-cftr-function
#15
Elizabeth L Kramer, William D Hardie, Satish K Madala, Cynthia R Davidson, John Paul Clancy
BACKGROUND: Cystic fibrosis (CF) produces variable lung disease phenotypes that are in part independent of CFTR genotype. Transforming growth factor beta (TGFβ) is the best described genetic modifier of the CF phenotype, but its mechanism of action is unknown. We hypothesized that TGFβ is sufficient to drive pathognomonic features of CF lung disease in vivo and that CFTR deficiency enhances susceptibility to pathologic TGFβ effects. METHODS: A CF mouse model and littermate controls were exposed intratracheally to an adenoviral vector containing the TGFβ1 cDNA (Ad-TGFβ), empty vector, or PBS only...
June 7, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29847991/activated-na%C3%A3-ve-b-cells-promote-development-of-malignant-pleural-effusion-by-different-regulation-of-th1-and-th17-response
#16
Xiu-Zhi Wu, Xin-Yu Shi, Kan Zhai, Feng-Shuang Yi, Zhen Wang, Wen Wang, Xue-Bin Pei, Li-Li Xu, Zheng Wang, Huan-Zhong Shi
Inflammatory signaling networks between tumor cells and immune cells contribute to the development of malignant pleural effusion (MPE). B cells have been found in MPE, however, little is known about their roles there. In the present study, by using mouse MPE models, we noted that although the total B cells in MPE were decreased as compared to the corresponding blood and spleen, the percentage of activated naïve B cells expressing higher levels of CD80, CD86, MHC-II, CD44, CD69, and PD-L1 molecules were increased in wild type mouse MPE...
May 31, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29847990/pregnancy-preserves-pulmonary-function-following-influenza-virus-infection-in-c57bl-6-mice
#17
Meghan S Vermillion, Andrew Nelson, Landon G Vom Steeg, Jeffrey Martin Loube, Wayne Mitzner, Sabra L Klein
Pregnancy is associated with significant anatomic and functional changes to the cardiopulmonary system. Using pregnant C57BL/6 mice, we characterized changes in pulmonary structure and function during pregnancy in healthy animals and following infection with influenza A virus (IAV). We hypothesized that pregnancy-associated alterations in pulmonary physiology would contribute to the more severe outcome of IAV infection. Nonpregnant and pregnant females (at embryonic day 10.5) were either mock-infected or infected with 2009 H1N1 IAV for assessment of pulmonary function, structure, and inflammation at 8 days post-inoculation...
May 31, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29847989/inhalation-of-electronic-cigarette-aerosol-induces-reflex-bronchoconstriction-by-activation-of-vagal-bronchopulmonary-c-fibers
#18
Mehdi Khosravi, Ruei-Lung Lin, Lu-Yuan Lee
The electronic cigarette (e-cig) has been suggested as a safer alternative to tobacco cigarettes. However, the health effects of e-cig in the airways have not been fully investigated. Nicotine, the primary chemical constituent of the e-cig aerosol, has been shown to stimulate vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit vigorous pulmonary defense reflexes, including airway constriction. In this study, we investigated the bronchomotor response to e-cig inhalation challenge in anesthetized guinea pigs and the mechanisms involved in regulating these responses...
May 31, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29792349/pulmonary-endothelial-permeability-and-tissue-fluid-balance-depend-on-the-viscosity-of-the-perfusion-solution
#19
Simon C Rowan, Keith D Rochfort, Lucie Piouceau, Philip M Cummins, Malachy O'Rourke, Paul McLoughlin
Fluid filtration in the pulmonary microcirculation depends on the hydrostatic and oncotic pressure gradients across the endothelium, and the selective permeability of the endothelial barrier. Maintaining normal fluid balance depends both on specific properties of the endothelium and of the perfusing blood. Although some of the essential properties of blood needed to prevent excessive fluid leak have been identified and characterised, our understanding of these remains incomplete. The role of perfusate viscosity in maintaining normal fluid exchange has not previously been examined...
May 24, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29792348/cell-division-cycle-7-kinase-is-a-negative-regulator-of-cell-mediated-collagen-degradation
#20
Michael Jeffrey Podolsky, Deepti Gupta, Arnold Ha, Ryan Ta, Amin Khalifeh-Soltani, William McKleroy, Ritwik Datta, Dean Sheppard, Kamran Atabai
Although extensive work has delineated many of the mechanisms of extracellular matrix (ECM) production, far less is known about pathways that regulate ECM degradation. This is particularly true of cellular internalization and degradation of matrix, which play an underappreciated role in ECM metabolism and lung fibrosis. For example, genetic perturbation of this pathway leads to exacerbated fibrosis in experimental animal models. In this work, we present the results of an unbiased screen of Drosophila phagocytes that yielded multiple genes that when silenced led to increased collagen uptake...
May 24, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
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