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Alveolar epithelial injury and repair

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https://www.readbyqxmd.com/read/28916766/stimulatory-secretions-of-airway-epithelial-cells-accelerate-early-repair-of-tracheal-epithelium
#1
Egi Kardia, Rafeezul Mohamed, Badrul Hisham Yahaya
Airway stem/progenitor epithelial cells (AECs) are notable for their differentiation capacities in response to lung injury. Our previous finding highlighted the regenerative capacity of AECs following transplantation in repairing tracheal injury and reducing the severity of alveolar damage associated acute lung injury in a rabbit model. The goal of this study is to further investigate the potential of AECs to re-populate the tracheal epithelium and to study their stimulatory effect on inhibiting pro-inflammatory cytokines, epithelial cell migration and proliferation, and epithelial-to-mesenchymal transition (EMT) process following tracheal injury...
September 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28905450/nrf2-transfection-enhances-the-efficacy-of-human-amniotic-mesenchymal-stem-cells-to-repair-lung-injury-induced-by-lipopolysaccharide
#2
Shouqin Zhang, Wei Jiang, Lijie Ma, Yuhao Liu, Xiangyu Zhang, Sheng Wang
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are clinical emergencies with no effective pharmaceutical treatment. This study aims to determine the protective effects of Nrf2-transfected human amniotic mesenchymal stem cells (hAMSCs) against lipopolysaccharide (LPS)-induced lung injury in mice. hAMSCs stably transfected with Nrf2 or green fluorescent protein control were transplanted into male C57BL/6 mice via the tail vein 4 h after intratracheal instillation of LPS. At 3, 7 and 14 days after cell transplantation, total lung injury score (the Smith score) was determined by hematoxylin and eosin staining...
September 14, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28886383/anatomically-and-functionally-distinct-lung-mesenchymal-populations-marked-by-lgr5-and-lgr6
#3
Joo-Hyeon Lee, Tuomas Tammela, Matan Hofree, Jinwook Choi, Nemanja Despot Marjanovic, Seungmin Han, David Canner, Katherine Wu, Margherita Paschini, Dong Ha Bhang, Tyler Jacks, Aviv Regev, Carla F Kim
The diversity of mesenchymal cell types in the lung that influence epithelial homeostasis and regeneration is poorly defined. We used genetic lineage tracing, single-cell RNA sequencing, and organoid culture approaches to show that Lgr5 and Lgr6, well-known markers of stem cells in epithelial tissues, are markers of mesenchymal cells in the adult lung. Lgr6(+) cells comprise a subpopulation of smooth muscle cells surrounding airway epithelia and promote airway differentiation of epithelial progenitors via Wnt-Fgf10 cooperation...
September 7, 2017: Cell
https://www.readbyqxmd.com/read/28878195/1-945-25-dihydroxyvitamin-d3-attenuates-tgf-946-induced-pro-fibrotic-effects-in-human-lung-epithelial-cells-through-inhibition-of-epithelial-mesenchymal-transition
#4
Fei Jiang, Yong Yang, Lian Xue, Bingyan Li, Zengli Zhang
Pulmonary fibrosis is a progressive fibrotic lung disease of persisting lung injury and ineffective wound repair, with poor prognosis. Epithelial-mesenchymal transition (EMT) of alveolar epithelia cells is an early event in the development of pulmonary fibrosis, and transforming growth factor β (TGF-β) is an acknowledged inducer of EMT. Epidemiological studies demonstrated that serum levels of 25-hydroxy-vitamin D were associated with the presence of fibrosis diseases. We investigated whether vitamin D attenuated TGF-β-induced pro-fibrotic effects through inhibiting EMT in human alveolar epithelia A549 cells...
September 6, 2017: Nutrients
https://www.readbyqxmd.com/read/28799781/microrna-29c-prevents-pulmonary-fibrosis-by-regulating-epithelial-cell-renewal-and-apoptosis
#5
Ting Xie, Jiurong Liang, Yan Geng, Ningshan Liu, Adrianne Kurkciyan, Vrishika Kulur, Dong Leng, Nan Deng, Zhenqiu Liu, Jianbo Song, Peter Chen, Paul W Noble, Dianhua Jiang
Successful repair and renewal of alveolar epithelial cells are critical in prohibiting the accumulation of myofibroblasts in pulmonary fibrogenesis. MicroRNAs (miRNAs) are multi-focal regulators involved in lung injury and repair. But the contribution of miRNAs to AEC2 renewal and apoptosis is incompletely understood. We report that microRNA-29c (MiR-29c) expression is lower in AEC2s of individuals with idiopathic pulmonary fibrosis (IPF) than healthy lungs. Epithelial cells overexpressing miR-29c show higher proliferative rate and viability...
August 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28775380/rage-inhibition-reduces-acute-lung-injury-in-mice
#6
Raiko Blondonnet, Jules Audard, Corinne Belville, Gael Clairefond, Jean Lutz, Damien Bouvier, Laurence Roszyk, Christelle Gross, Marilyne Lavergne, Marianne Fournet, Loic Blanchon, Caroline Vachias, Christelle Damon-Soubeyrand, Vincent Sapin, Jean-Michel Constantin, Matthieu Jabaudon
The receptor for advanced glycation end-products (RAGE) is involved in inflammatory response during acute respiratory distress syndrome (ARDS). Growing body of evidence support strategies of RAGE inhibition in experimental lung injury, but its modalities and effects remain underinvestigated. Anesthetised C57BL/6JRj mice were divided in four groups; three of them underwent orotracheal instillation of acid and were treated with anti-RAGE monoclonal antibody (mAb) or recombinant soluble RAGE (sRAGE), acting as a decoy receptor...
August 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28775044/senolytic-drugs-target%C3%A2-alveolar-epithelial-cell-function-and-attenuate-experimental-lung-fibrosis-ex-vivo
#7
Mareike Lehmann, Martina Korfei, Kathrin Mutze, Stephan Klee, Wioletta Skronska-Wasek, Hani N Alsafadi, Chiharu Ota, Rita Costa, Herbert B Schiller, Michael Lindner, Darcy E Wagner, Andreas Günther, Melanie Königshoff
Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with poor prognosis and limited therapeutic options. The incidence of IPF increases with age, and ageing-related mechanisms such as cellular senescence have been proposed as pathogenic drivers. The lung alveolar epithelium represents a major site of tissue injury in IPF and senescence of this cell population is probably detrimental to lung repair. However, the potential pathomechanisms of alveolar epithelial cell senescence and the impact of senolytic drugs on senescent lung cells and fibrosis remain unknown...
August 2017: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/28760550/the-role-of-c-ebp%C3%AE-phosphorylation-in-modulating-membrane-phospholipids-repairing-in-lps-induced-human-lung-bronchial-epithelial-cells
#8
Shiyu Shu, Yan Xu, Ling Xie, Yufang Ouyang
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a common critical emergency with high mortality in clinical practice. The key mechanism of ALI/ARDS is that the excessive inflammatory response damages the integrity of alveolar and bronchial cell membrane and thus affects their basic function. Phospholipids are the main component of cell membranes. Phospholipase A2 (PLA2), which catalyzes the cleavage of membrane phospholipids, is the most important inflammatory mediator of ALI. However, clara cell secretory protein 1 (CCSP1), an endogenous PLA2 inhibitor can increase the self-defense of membrane phospholipids...
September 20, 2017: Gene
https://www.readbyqxmd.com/read/28732066/inhibition-of-pulmonary-%C3%AE-carotene-15-15-oxygenase-expression-by-glucocorticoid-involves-ppar%C3%AE
#9
Xiaoming Gong, Raju Marisiddaiah, Lewis P Rubin
β-carotene 15,15'-oxygenase (BCO1) catalyzes the first step in the conversion of dietary provitamin A carotenoids to vitamin A. This enzyme is expressed in a variety of developing and adult tissues, suggesting that its activity may regulate local retinoid synthesis. Vitamin A and related compounds (retinoids) are critical regulators of lung epithelial development, integrity, and injury repair. A balance between the actions of retinoids and glucocorticoids (GCs) promotes normal lung development and, in particular, alveolarization...
2017: PloS One
https://www.readbyqxmd.com/read/28662821/the-role-of-matrix-metalloproteinases-in-development-repair-and-destruction-of-the-lungs
#10
Amanda Y Hendrix, Farrah Kheradmand
Normal gas exchange after birth requires functional lung alveolar units that are lined with epithelial cells, parts of which are intricately fused with microvascular capillaries. A significant phase of alveolar lung development occurs in the perinatal period, continues throughout early stages in life, and requires activation of matrix-remodeling enzymes. Failure to achieve an optimum number of alveoli during lung maturation can cause several untoward medical consequences including disabling obstructive and/or restrictive lung diseases that limit physiological endurance and increase mortality...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28657777/epithelial-deletion-of-sulf2-exacerbates-bleomycin-induced-lung-injury-inflammation-and-mortality
#11
Xinping Yue
Epithelial injury has been proposed to be the initiating factor in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We have shown previously that heparan sulfate (HS) 6-O-endosulfatase 2 (Sulf2) is overexpressed in the hyperplastic type II alveolar epithelial cells (AECs) in the IPF lungs. By removing 6-O-sulfates from specific HS intra-chain sites, Sulf2 modulates the functions of many growth factors and cytokines. In this study we hypothesized that Sulf2 plays a regulatory role in alveolar epithelial injury and repair, using the murine bleomycin model...
June 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28618253/hypoxia-inducible-factor-1%C3%AE-signaling-promotes-repair-of-the-alveolar-epithelium-after-acute-lung-injury
#12
Jazalle McClendon, Nicole L Jansing, Elizabeth F Redente, Aneta Gandjeva, Yoko Ito, Sean P Colgan, Aftab Ahmad, David W H Riches, Harold A Chapman, Robert J Mason, Rubin M Tuder, Rachel L Zemans
During the acute respiratory distress syndrome, epithelial cells, primarily alveolar type (AT) I cells, die and slough off, resulting in enhanced permeability. ATII cells proliferate and spread onto the denuded basement membrane to reseal the barrier. Repair of the alveolar epithelium is critical for clinical recovery; however, mechanisms underlying ATII cell proliferation and spreading are not well understood. We hypothesized that hypoxia-inducible factor (HIF)1α promotes proliferation and spreading of ATII cells during repair after lung injury...
August 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28587419/regulation-of-the-angiotensin-ii-p22phox-reactive-oxygen-species-signaling-pathway-apoptosis-and-8-oxoguanine-dna-glycosylase-1-retrieval-in-hyperoxia-induced-lung-injury-and-fibrosis-in-rats
#13
Yu Wang, Yuxi Zhu, Yudi Zhu, Zhongyi Lu, Feng Xu
The present study was designed to explore the impact of hyperoxia on lung injury and fibrosis via the angiotensin II (AngII)-p22phox-reactive oxygen species (ROS) signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 (OGG1) repair enzyme. Newborn Sprague-Dawley rats were randomly divided in the newborn air group, newborn hyperoxia group and newborn intervention group, the latter of which was administered the chymotrypsin inhibitor, 2-(5-formylamino-6-oxo-2-phenyl-1, 6-dihydropyrimidine-1-yl)-N-[4-dioxo-1-phenyl-7-(2-pyridyloxy)] 2-heptyl-acetamide (NK3201)...
June 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28586241/unbiased-quantitation-of-atii-to-ati-cell-transdifferentiation-during-repair-after-lung-injury-in-mice
#14
Nicole L Jansing, Jazalle McClendon, Peter M Henson, Rubin M Tuder, Dallas M Hyde, Rachel L Zemans
The alveolar epithelium consists of squamous alveolar type (AT)I and cuboidal ATII cells. ATI cells cover 95-98% of the alveolar surface, thereby playing a critical role in barrier integrity, and are extremely thin, thus permitting efficient gas exchange. During lung injury, ATI cells die, resulting in increased epithelial permeability. ATII cells reepithelialize the alveolar surface via proliferation and transdifferentiation into ATI cells. Transdifferentiation is characterized by downregulation of ATII cell markers, upregulation of ATI cell markers, and cell spreading resulting in a change in morphology from cuboidal to squamous, thus restoring normal alveolar architecture and function...
June 6, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28526890/a-heteromeric-molecular-complex-regulates-the-migration-of-lung-alveolar-epithelial-cells-during-wound-healing
#15
Manik C Ghosh, Patrudu S Makena, Joseph Kennedy, Bin Teng, Charlean Luellen, Scott E Sinclair, Christopher M Waters
Alveolar type II epithelial cells (ATII) are instrumental in early wound healing in response to lung injury, restoring epithelial integrity through spreading and migration. We previously reported in separate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor CXCR4 promote epithelial repair mechanisms. However, potential interactions between these two pathways were not previously considered. In the present study, we found that wounding of rat ATII cells promoted increased association between FAK and CXCR4...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28417017/galectin-1-inhibition-attenuates-profibrotic-signaling-in-hypoxia-induced-pulmonary-fibrosis
#16
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/28402849/uroplakin-3a-cells-are-a-distinctive-population-of-epithelial-progenitors-that-contribute-to-airway-maintenance-and-post-injury-repair
#17
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/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, Xue-Ke Zhao, Nathaniel Bone, Ashish R Kurundkar, Louise Hecker, Meng Hu, Yong Zhou, Jeffrey C 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 response 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 transforming growth factor-β1 (TGF-β1). Rat type II alveolar epithelial cells (RLE-6TN) were treated with or without TGF-β1, and the expressions of mesenchymal markers, phenotype, and function were analyzed...
June 1, 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
#19
Hani N Alsafadi, Claudia A Staab-Weijnitz, Mareike Lehmann, Michael Lindner, Britta Peschel, Melanie Königshoff, Darcy E Wagner
Idiopathic pulmonary fibrosis (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 that 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)...
June 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28296468/foxp3-regulatory-t-cell-expression-of-keratinocyte-growth-factor-enhances-lung-epithelial-proliferation
#20
Catherine F Dial, Miriya K Tune, Claire M Doerschuk, Jason R Mock
Repair of the lung epithelium after injury is a critical component for resolution; however, the processes necessary to drive epithelial resolution are not clearly defined. Published data demonstrate that Foxp3(+) regulatory T cells (Tregs) enhance alveolar epithelial proliferation after injury, and Tregs in vitro directly promote type II alveolar epithelial cell (AT2) proliferation, in part by a contact-independent mechanism. Therefore, we sought to determine the contribution of Treg-specific expression of a growth factor that is known to be important in lung repair, keratinocyte growth factor (kgf)...
August 2017: American Journal of Respiratory Cell and Molecular Biology
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