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Alveolar epithelial injury

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https://www.readbyqxmd.com/read/28428003/rac1-signaling-regulates-cigarette-smoke-induced-inflammation-in-the-lung-via-the-erk1-2-mapk-and-stat3-pathways
#1
Jun-Xia Jiang, Shui-Juan Zhang, Hui-Juan Shen, Yan Guan, Qi Liu, Wei Zhao, Yong-Liang Jia, Jian Shen, Xiao-Feng Yan, Qiang-Min Xie
Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Our previous studies have indicated that Rac1 is involved in lipopolysaccharide-induced pulmonary injury and CS-mediated epithelial-mesenchymal transition. However, the contribution of Rac1 activity to CS-induced lung inflammation remains not fully clear. In this study, we investigated the regulation of Rac1 in CS-induced pulmonary inflammation. Mice or 16HBE cells were exposed to CS or cigarette smoke extract (CSE) to induce acute inflammation...
April 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28427999/serpinb1-ameliorates-acute-lung-injury-in-liver-transplantation-through-erk1-2-mediated-stat3-dependent-ho-1-induction
#2
Weifeng Yao, Haobo Li, Gangjian Luo, Xiang Li, Chaojin Chen, Dongdong Yuan, Xinjin Chi, Zhengyuan Xia, Ziqing Hei
BACKGROUND: Postoperative acute lung injury(ALI) is a severe complication after liver transplantation, which severely affects postoperative patients' survival. The underlying mechanism is largely unknown and effective treatment limited. We explored the role of serpin protease inhibitor B1(SERPINB1), a potent inhibitor of neutrophil serine proteases, in ALI in liver transplantation and its interplay with signal transducer and activator of transcription 3(STAT3) and heme oxygenase-1(HO-1)...
April 17, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28426693/influence-of-prenatal-hypoxia-and-postnatal-hyperoxia-on-morphologic-lung-maturation-in-mice
#3
Andreas Schmiedl, Torge Roolfs, Erol Tutdibi, Ludwig Gortner, Dominik Monz
BACKGROUND: Oxygen supply as a lifesaving intervention is frequently used to treat preterm infants suffering additionally from possible prenatal or perinatal pathogen features. The impact of oxygen and/or physical lung injury may influence the morphological lung development, leading to a chronic postnatal lung disease called bronchopulmonary dysplasia (BPD). At present different experimental BPD models are used. However, there are no systematic comparative studies regarding different influences of oxygen on morphological lung maturation...
2017: PloS One
https://www.readbyqxmd.com/read/28426531/high-fat-feeding-protects-mice-from-ventilator-induced-lung-injury-via-neutrophil-independent-mechanisms
#4
Michael R Wilson, Joanne E Petrie, Michael W Shaw, Cong Hu, Charlotte M Oakley, Samantha J Woods, Brijesh V Patel, Kieran P O'Dea, Masao Takata
OBJECTIVE: Obesity has a complex impact on acute respiratory distress syndrome patients, being associated with increased likelihood of developing the syndrome but reduced likelihood of dying. We propose that such observations are potentially explained by a model in which obesity influences the iatrogenic injury that occurs subsequent to intensive care admission. This study therefore investigated whether fat feeding protected mice from ventilator-induced lung injury. DESIGN: In vivo study...
April 19, 2017: Critical Care Medicine
https://www.readbyqxmd.com/read/28417017/galectin-1-inhibition-attenuates-profibrotic-signaling-in-hypoxia-induced-pulmonary-fibrosis
#5
Jaymin J Kathiriya, Niyati Nakra, Jenna Nixon, Puja S Patel, Vijay Vaghasiya, Ahmed Alhassani, Zhi Tian, Diane Allen-Gipson, Vrushank Davé
Idiopathic pulmonary fibrosis (IPF) is characterized by lung remodeling arising from epithelial injury, aberrant fibroblast growth, and excessive deposition of extracellular matrix. Repeated epithelial injury elicits abnormal wound repair and lung remodeling, often associated with alveolar collapse and edema, leading to focal hypoxia. Here, we demonstrate that hypoxia is a physiological insult that contributes to pulmonary fibrosis (PF) and define its molecular roles in profibrotic activation of lung epithelial cells...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28413775/an-interesting-case-of-mycoplasma-pneumonia-associated-multisystem-involvement-and-diffuse-alveolar-hemorrhage
#6
Rashmi Mishra, Edison Cano, Sindhaghatta Venkatram, Gilda Diaz-Fuentes
Severe mycoplasma pneumonia is a rare entity with only 0.5-2% of cases having a fulminant course. We present a 74-year-old woman with hypertension, diabetes mellitus and remote history of marginal zone B-cell lymphoma admitted with abdominal pain and diarrhea of 1-2 days associated with body-aches, dyspnea, dry cough and weight loss for 2-3 weeks. On physical exam, she was febrile, tachypneic, tachycardic and hypoxic on room air. Chest examination revealed diffuse crackles and end-expiratory wheezes. Laboratory tests showed anemia, acute-on-chronic kidney injury and hyaline casts and epithelial cells in the urine analysis...
2017: Respiratory Medicine Case Reports
https://www.readbyqxmd.com/read/28413467/calcitonin-gene-related-peptide-protects-type-ii-alveolar-epithelial-cells-from-hyperoxia-induced-dna-damage-and-cell-death
#7
Hongmin Fu, Tiesong Zhang, Rongwei Huang, Zhen Yang, Chunming Liu, Ming Li, Fang Fang, Feng Xu
Hyperoxia therapy for acute lung injury (ALI) may unexpectedly lead to reactive oxygen species (ROS) production and cause additional ALI. Calcitonin gene-related peptide (CGRP) is a 37 amino acid neuropeptide that regulates inflammasome activation. However, the role of CGRP in DNA damage during hyperoxia is unclear. Therefore, the aim of the present study was to investigate the effects of CGRP on DNA damage and the cell death of alveolar epithelial type II cells (AEC II) exposed to 60% oxygen. AEC II were isolated from 19-20 gestational day fetal rat lungs and were exposed to air or to 60% oxygen during treatment with CGRP or the specific CGRP receptor antagonist CGRP8-37...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28402849/uroplakin-3a-cells-are-a-distinctive-population-of-epithelial-progenitors-that-contribute-to-airway-maintenance-and-post-injury-repair
#8
Arjun Guha, Aditya Deshpande, Aradhya Jain, Paola Sebastiani, Wellington V Cardoso
There is evidence that certain club cells (CCs) in the murine airways associated with neuroepithelial bodies (NEBs) and terminal bronchioles are resistant to the xenobiotic naphthalene (Nap) and repopulate the airways after Nap injury. The identity and significance of these progenitors (variant CCs, v-CCs) have remained elusive. A recent screen for CC markers identified rare Uroplakin3a (Upk3a)-expressing cells (U-CCs) with a v-CC-like distribution. Here, we employ lineage analysis in the uninjured and chemically injured lungs to investigate the role of U-CCs as epithelial progenitors...
April 11, 2017: Cell Reports
https://www.readbyqxmd.com/read/28397939/recent-insight-into-potential-acute-respiratory-distress-syndrome
#9
Zulkifli Amin, Fitriana N Rahmawati
Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury, characterized by increased pulmonary capillary endothelial cells and alveolar epithelial cells permeability leading to respiratory failure in the absence of cardiac failure. Despite recent advances in treatments, the overall mortality because of ARDS remains high. Biomarkers may help to diagnose, predict the severity, development, and outcome of ARDS in order to improve patient care and decrease morbidity and mortality. This review will focus on soluble receptor for advanced glycation end-products, soluble tumor necrosis factor-receptor 1, Interluken-6 (IL-6), IL-8, and plasminogen activator inhibitor-1, which have a greater potential based on recent studies...
April 2017: Saudi Medical Journal
https://www.readbyqxmd.com/read/28396150/irisin-mediated-protective-effect-on-lps-induced-acute-lung-injury-via-suppressing-inflammation-and-apoptosis-of-alveolar-epithelial-cells
#10
Lei Shao, Di Meng, Fei Yang, Haibo Song, Dongqi Tang
It is considered that the essence of acute lung injury (ALI) is an excessive and uncontrolled inflammatory response in lung, of which mainly is attributed to the release of inflammatory mediators. Recent studies demonstrated that irisin, which is a metabolism associated factor after physical exercise could suppression of inflammation by regulating cellular signaling pathways, however, the underlying molecular mechanism remains to be determined. The present study aimed to reveal the potential mechanism responsible for the anti-inflammatory effects of irisin on LPS-induced acute lung injury in mice and in A549 cells...
April 7, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28394655/stretch-induced-apoptosis-in-rat-alveolar-epithelial-cells-is-mediated-by-the-intrinsic-mitochondrial-pathway
#11
Hartmut Kuhn, Hendrik Nieuwenhuijsen, Bianca Karthe, Hubert Wirtz
BACKGROUND: Alveolar type II (ATII) cells in the lung are exposed to mechanical stretch during breathing and mechanical ventilation. Increased mechanical stretch contributes to lung injury by induction of apoptosis and necrosis in ATII cells. AIM OF THE STUDY: In this study, we investigated the intrinsic and the extrinsic apoptosis pathways, and their involvement in our model of stretch-induced apoptosis. MATERIAL AND METHODS: ATII cells were stretched on elastic membranes for 24 h and apoptosis was determined at different time points...
February 2017: Experimental Lung Research
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
#12
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/28384256/probucol-attenuates-hyperoxia-induced-lung-injury-in-mice
#13
Tomonobu Kawaguchi, Toyoshi Yanagihara, Tetsuya Yokoyama, Saiko Suetsugu-Ogata, Naoki Hamada, Chika Harada-Ikeda, Kunihiro Suzuki, Takashige Maeyama, Kazuyoshi Kuwano, Yoichi Nakanishi
Hyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death, and proinflammatory cytokines are thought to be involved. Probucol-a commercially available drug for treating hypercholesterolemia-has been suggested to have antioxidant and antiapoptotic effects. This study aimed to assess whether probucol could attenuate hyperoxic lung injury in mice...
2017: PloS One
https://www.readbyqxmd.com/read/28365871/cavidine-ameliorates-lipopolysaccharide-induced-acute-lung-injury-via-nf-%C3%AE%C2%BAb-signaling-pathway-in-vivo-and-in-vitro
#14
Xiaofeng Niu, Fang Liu, Weifeng Li, Wenbing Zhi, Hailin Zhang, Xiumei Wang, Zehong He
Acute lung injury (ALI) is characterized by widespread inflammation in the lungs and alveolar-capillary destruction, causing high morbidity and mortality. Cavidine, isolated from Corydalis impatiens, have been exhibited to have potent anti-inflammatory effects in previous studies. The purpose of this study was to evaluate the protective effect of cavidine on lipopolysaccharide (LPS)-induced ALI and to enunciate the underlying in vivo and in vitro mechanisms. Mice were intraperitoneally administrated with cavidine (1, 3, or 10 mg/kg) at 1 and 12 h, prior to the induction of ALI by intranasal administration of LPS (30 mg/kg)...
April 1, 2017: Inflammation
https://www.readbyqxmd.com/read/28363030/integrated-stress-response-mediates-epithelial-injury-in-mechanical-ventilation
#15
Tamas Dolinay, Blanca E Himes, Maya Shumyatcher, Gladys Gray Lawrence, Susan S Margulies
RATIONALE: Ventilator-induced lung injury (VILI) is a severe complication of mechanical ventilation that can lead to acute respiratory distress syndrome (ARDS). VILI is characterized by damage to the epithelial barrier with subsequent pulmonary edema and profound hypoxia. Available lung protective ventilator strategies offer only modest benefit in preventing VILI because they cannot impede alveolar overdistension and concomitant epithelial barrier dysfunction in the inflamed lung regions...
March 31, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28360109/focal-adhesion-kinase-signaling-determines-the-fate-of-lung-epithelial-cells-in-response-to-tgf-%C3%AE
#16
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/28340238/cigarette-smoke-exposure-worsens-endotoxin-induced-lung-injury-and-pulmonary-edema-in-mice
#17
Jeffrey E Gotts, Jason Abbott, Xiaohui Fang, Haru Yanagisawa, Naoki Takasaka, Stephen L Nishimura, Carolyn S Calfee, Michael A Matthay
Introduction: Cigarette smoking (CS) remains a major public health concern and has recently been associated with an increased risk of developing acute respiratory distress syndrome (ARDS). Bronchoalveolar lavage (BAL) experiments in human volunteers have demonstrated that active smokers develop increased alveolar-epithelial barrier permeability to protein after inhaling lipopolysaccharide (LPS). Here we tested the hypothesis that short-term whole-body CS exposure would increase LPS-induced lung edema in mice...
March 9, 2017: Nicotine & Tobacco Research: Official Journal of the Society for Research on Nicotine and Tobacco
https://www.readbyqxmd.com/read/28323898/perfluorocarbon-reduces-cell-damage-from-blast-injury-by-inhibiting-signal-paths-of-nf-%C3%AE%C2%BAb-mapk-and-bcl-2-bax-signaling-pathway-in-a549-cells
#18
Zhaorui Zhang, Zhixin Liang, Huaidong Li, Chunsun Li, Zhen Yang, Yanqin Li, Danyang She, Lu Cao, Wenjie Wang, Changlin Liu, Liangan Chen
BACKGROUND AND OBJECTIVE: Blast lung injury is a common type of blast injury and has very high mortality. Therefore, research to identify medical therapies for blast injury is important. Perfluorocarbon (PFC) is used to improve gas exchange in diseased lungs and has anti-inflammatory functions in vitro and in vivo. The aim of this study was to determine whether PFC reduces damage to A549 cells caused by blast injury and to elucidate its possible mechanisms of action. STUDY DESIGN AND METHODS: A549 alveolar epithelial cells exposed to blast waves were treated with and without PFC...
2017: PloS One
https://www.readbyqxmd.com/read/28321785/microrna-34a-suppresses-autophagy-in-alveolar-type-ii-epithelial-cells-in-acute-lung-injury-by-inhibiting-foxo3-expression
#19
Lan Song, Fangliang Zhou, Lijuan Cheng, Mei Hu, Yingchun He, Bo Zhang, Duanfang Liao, Zhaojun Xu
Excessive autophagic activity of alveolar type II epithelial (AT-II) cells is one of the main causes of acute lung injury (ALI); however, the underlying molecular mechanism remains to be determined. The microRNAs (miRNAs) are involved with autophagy in many diseases. The objective of this study was therefore to investigate the relationship between the miRNA expression and the autophagic activity of the AT-II cells in the pathogenesis of ALI and its molecular mechanism. A mouse model of ALI and AT-II cell injury was induced using lipopolysaccharide (LPS) in vivo and in vitro, and the expression of miR-34a and the autophagy-related proteins LC3 II/I and p62 were determined...
March 21, 2017: Inflammation
https://www.readbyqxmd.com/read/28314802/an-ex-vivo-model-to-induce-early-fibrosis-like-changes-in-human-precision-cut-lung-slices
#20
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
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