keyword
MENU ▼
Read by QxMD icon Read
search

Alveolar epithelial injury and repair

keyword
https://www.readbyqxmd.com/read/29731780/lung-mesenchymal-stem-cells-ameliorate-elastase-induced-damage-in-an-animal-model-of-emphysema
#1
Donato Cappetta, Antonella De Angelis, Giuseppe Spaziano, Gioia Tartaglione, Elena Piegari, Grazia Esposito, Loreta Pia Ciuffreda, Angela Liparulo, Manuela Sgambato, Teresa Palmira Russo, Francesco Rossi, Liberato Berrino, Konrad Urbanek, Bruno D'Agostino
Pulmonary emphysema is a respiratory condition characterized by alveolar destruction that leads to airflow limitation and reduced lung function. Although with extensive research, the pathophysiology of emphysema is poorly understood and effective treatments are still missing. Evidence suggests that mesenchymal stem cells (MSCs) possess the ability to engraft the injured tissues and induce repair via a paracrine effect. Thus, the aim of this study was to test the effects of the intratracheal administration of lung-derived mouse MSCs in a model of elastase-induced emphysema...
2018: Stem Cells International
https://www.readbyqxmd.com/read/29722336/mitochondrial-autophagy-and-nlrp3-inflammasome-in-pulmonary-tissues-from-severe-combined-immunodeficient-mice-after-cardiac-arrest-and-cardiopulmonary-resuscitation
#2
Jing-Jun Lyu, Jawahar L Mehta, Yi Li, Lu Ye, Sheng-Nan Sun, Hong-Shuang Sun, Jia-Chang Li, Dong-Mei Zhang, Jie Wei
Background: The incidence of cancer, diabetes, and autoimmune diseases has been increasing. Furthermore, there are more and more patients with solid organ transplants. The survival rate of these immunocompromised individuals is extremely low when they are severely hit-on. In this study, we established cardiac arrest cardiopulmonary resuscitation (CPR) model in severe combined immunodeficient (SCID) mice, analyzed the expression and activation of mitochondrial autophagy and NLRP3 inflammasome/caspase-1, and explored mitochondrial repair and inflammatory injury in immunodeficiency individual during systemic ischemia-reperfusion injury...
May 20, 2018: Chinese Medical Journal
https://www.readbyqxmd.com/read/29664060/specialized-pro-resolving-mediators-regulate-alveolar-fluid-clearance-during-acute-respiratory-distress-syndrome
#3
REVIEW
Qian Wang, Song-Fan Yan, Yu Hao, Sheng-Wei Jin
Objective: Acute respiratory distress syndrome (ARDS) is an acute and lethal clinical syndrome that is characterized by the injury of alveolar epithelium, which impairs active fluid transport in the lung, and impedes the reabsorption of edema fluid from the alveolar space. This review aimed to discuss the role of pro-resolving mediators on the regulation of alveolar fluid clearance (AFC) in ARDS. Data Sources: Articles published up to September 2017 were selected from the PubMed, with the keywords of "alveolar fluid clearance" or "lung edema" or "acute lung injury" or "acute respiratory distress syndrome", and "specialized pro-resolving mediators" or "lipoxin" or "resolvin" or "protectin" or "maresin" or "alveolar epithelial cells" or "aspirin-triggered lipid mediators" or "carbon monoxide and heme oxygenase" or "annexin A1"...
April 20, 2018: Chinese Medical Journal
https://www.readbyqxmd.com/read/29625013/successful-establishment-of-primary-type-2-alveolar-epithelium-with-3d-organotypic-co-culture
#4
Jennifer M S Sucre, Christopher S Jetter, Holli Loomans, Janice Williams, Erin J Plosa, John T Benjamin, Lisa R Young, Jonathan A Kropski, Carla L Calvi, Seunghyi Kook, Ping Wang, Linda Gleaves, Adel Eskaros, Laura Goetzl, Timothy S Blackwell, Susan H Guttentag, Andries Zijlstra
Alveolar type 2 (AT2) epithelial cells are uniquely specialized to produce surfactant in the lung and act as progenitor cells in the process of repair after lung injury. AT2 cell injury has been implicated in several lung diseases, including idiopathic pulmonary fibrosis and bronchopulmonary dysplasia. The inability to maintain primary AT2 cells in culture has been a significant barrier in the investigation of pulmonary biology. We have addressed this knowledge gap by developing a 3-dimensional organotypic co-culture using primary human fetal AT2 cells and pulmonary fibroblasts...
April 6, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29515024/identification-of-periplakin-as-a-major-regulator-of-lung-injury-and-repair-in-mice
#5
Valérie Besnard, Rania Dagher, Tania Madjer, Audrey Joannes, Madeleine Jaillet, Martin Kolb, Philippe Bonniaud, Lynne A Murray, Matthew A Sleeman, Bruno Crestani
Periplakin is a component of the desmosomes that acts as a cytolinker between intermediate filament scaffolding and the desmosomal plaque. Periplakin is strongly expressed by epithelial cells in the lung and is a target antigen for autoimmunity in idiopathic pulmonary fibrosis. The aim of this study was to determine the role of periplakin during lung injury and remodeling in a mouse model of lung fibrosis induced by bleomycin. We found that periplakin expression was downregulated in the whole lung and in alveolar epithelial cells following bleomycin-induced injury...
March 8, 2018: JCI Insight
https://www.readbyqxmd.com/read/29484847/lung-epithelial-specific-trip-1-overexpression-maintains-epithelial-integrity-during-hyperoxia-exposure
#6
Michael F Nyp, Sherry M Mabry, Angels Navarro, Heather Menden, Ricardo E Perez, Venkatesh Sampath, Ikechukwu I Ekekezie
The onset and degree of injury occurring in animals that develop hyperoxic acute lung injury (HALI) is dependent on age at exposure, suggesting that developmentally regulated pathways/factors must underlie initiation of the epithelial injury and subsequent repair. Type II TGFβ receptor interacting protein-1 (TRIP-1) is a negative regulator of TGFβ signaling, which we have previously shown is a developmentally regulated protein with modulatory effects on epithelial-fibroblastic signaling. The aim of this study was to assess if type II alveolar epithelial cells overexpressing TRIP-1 are protected against hyperoxia-induced epithelial injury, and in turn HALI...
March 2018: Physiological Reports
https://www.readbyqxmd.com/read/29471816/idiopathic-pulmonary-fibrosis-pathogenesis-and-management
#7
REVIEW
Giacomo Sgalla, Bruno Iovene, Mariarosaria Calvello, Margherita Ori, Francesco Varone, Luca Richeldi
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive disease characterized by the aberrant accumulation of fibrotic tissue in the lungs parenchyma, associated with significant morbidity and poor prognosis. This review will present the substantial advances achieved in the understanding of IPF pathogenesis and in the therapeutic options that can be offered to patients, and will address the issues regarding diagnosis and management that are still open. MAIN BODY: Over the last two decades much has been clarified about the pathogenic pathways underlying the development and progression of the lung scarring in IPF...
February 22, 2018: Respiratory Research
https://www.readbyqxmd.com/read/29458008/trefoil-factor-2-promotes-type-2-immunity-and-lung-repair-through-intrinsic-roles-in-hematopoietic-and-nonhematopoietic-cells
#8
Li-Yin Hung, Taylor K Oniskey, Debasish Sen, Matthew F Krummel, Andrew E Vaughan, Noam A Cohen, De'Broski R Herbert
Trefoil factors (TFFs) are small secreted proteins that regulate tissue integrity and repair at mucosal surfaces, particularly in the gastrointestinal tract. However, their relative contribution(s) to controlling baseline lung function or the extent of infection-induced lung injury are unknown issues. With the use of irradiation bone marrow chimeras, we found that TFF2 produced from both hematopoietic- and nonhematopoietic-derived cells is essential for host protection, proliferation of alveolar type 2 cells, and restoration of pulmonary gas exchange after infection with the hookworm parasite Nippostrongylus brasiliensis...
May 2018: American Journal of Pathology
https://www.readbyqxmd.com/read/29434764/pediatric-acute-respiratory-distress-syndrome-current-views
#9
Jinfeng Liu, Wei Wang, Fengli Liu, Zhenguang Li
Acute respiratory distress syndrome (ARDS) mainly involves acute respiratory failure. In addition to this affected patients feel progressive arterial hypoxemia, dyspnea, and a marked increase in the work of breathing. The only clinical solution for the above pathological state is ventilation. Mechanical ventilation is necessary to support life in ARDs but it itself worsen lung injury and the term is known clinically as 'ventilation induced lung injury' (VILI). At the cellular level, respiratory epithelial cells are subjected to cyclic stretch, i...
February 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29428947/a-combination-of-the-aerosolized-ppar-%C3%AE-agonist-pioglitazone-and-a-synthetic-surfactant-protein-b-peptide-mimic-prevents-hyperoxia-induced-neonatal-lung-injury-in-rats
#10
Reiko Sakurai, Cindy Lee, Humphrey Shen, Alan J Waring, Frans J Walther, Virender K Rehan
BACKGROUND: Despite improvements in perinatal care, bronchopulmonary dysplasia (BPD) in extremely premature infants has not decreased. Postnatal surfactant therapy provides symptomatic relief from respiratory distress syndrome, but does not translate into a reduction in BPD. Therefore, the search for effective interventions to prevent BPD continues. OBJECTIVES: Since PPAR-γ agonists have been demonstrated to promote neonatal lung maturation and injury repair, we hypothesized that a formulation of a PPAR-γ agonist, pioglitazone (PGZ) and a synthetic lung surfactant (a surfactant protein B peptide mimic, B-YL) combined would stimulate lung maturation and block hyperoxia-induced neonatal lung injury more effectively than either modality alone...
February 9, 2018: Neonatology
https://www.readbyqxmd.com/read/29400695/claudin-18-mediated-yap-activity-regulates-lung-stem-and-progenitor-cell-homeostasis-and-tumorigenesis
#11
Beiyun Zhou, Per Flodby, Jiao Luo, Dan R Castillo, Yixin Liu, Fa-Xing Yu, Alicia McConnell, Bino Varghese, Guanglei Li, Nyam-Osor Chimge, Mitsuhiro Sunohara, Michael N Koss, Wafaa Elatre, Peter Conti, Janice M Liebler, Chenchen Yang, Crystal N Marconett, Ite A Laird-Offringa, Parviz Minoo, Kunliang Guan, Barry R Stripp, Edward D Crandall, Zea Borok
Claudins, the integral tight junction (TJ) proteins that regulate paracellular permeability and cell polarity, are frequently dysregulated in cancer; however, their role in neoplastic progression is unclear. Here, we demonstrated that knockout of Cldn18, a claudin family member highly expressed in lung alveolar epithelium, leads to lung enlargement, parenchymal expansion, increased abundance and proliferation of known distal lung progenitors, the alveolar epithelial type II (AT2) cells, activation of Yes-associated protein (YAP), increased organ size, and tumorigenesis in mice...
March 1, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29386045/mesenchymal-stem-cell-based-therapy-for-radiation-induced-lung-injury
#12
REVIEW
Tiankai Xu, Yuyu Zhang, Pengyu Chang, Shouliang Gong, Lihong Shao, Lihua Dong
Since radiotherapy is widely used in managing thoracic tumors, physicians have begun to realize that radiation-induced lung injury (RILI) seriously limits the effects of radiotherapy. Unfortunately, there are still no effective methods for controlling RILI. Over the last few decades numerous studies have reported the beneficial effects of mesenchymal stem cells (MSCs) on tissue repair and regeneration. MSCs can not only differentiate into lung alveolar epithelial cells and secrete anti-inflammatory factors, but they also deliver some vehicles for gene therapy in repairing the injured lung, which provides new ideas for managing RILI...
January 31, 2018: Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/29331644/ozone-exposure-induces-respiratory-barrier-biphasic-injury-and-inflammation-controlled-by-il-33
#13
Chloé Michaudel, Claire Mackowiak, Isabelle Maillet, Louis Fauconnier, Cezmi A Akdis, Milena Sokolowska, Anita Dreher, Hern-Tze Tina Tan, Valérie F Quesniaux, Bernhard Ryffel, Dieudonnée Togbe
BACKGROUND: IL-33 plays a critical role in regulation of tissue homeostasis, injury, and repair. Whether IL-33 regulates neutrophil recruitment and functions independently of airways hyperresponsiveness (AHR) in the setting of ozone-induced lung injury and inflammation is unclear. OBJECTIVE: We sought to examine the role of the IL-33/ST2 axis in lung inflammation on acute ozone exposure in mice. METHODS: ST2- and Il33-deficient, IL-33 citrine reporter, and C57BL/6 (wild-type) mice underwent a single ozone exposure (1 ppm for 1 hour) in all studies...
January 10, 2018: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29321022/serum-metabolic-profiling-identified-a-distinct-metabolic-signature-in-patients-with-idiopathic-pulmonary-fibrosis-a-potential-biomarker-role-for-lysopc
#14
Barbara Rindlisbacher, Cornelia Schmid, Thomas Geiser, Cédric Bovet, Manuela Funke-Chambour
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease of unknown etiology. Patients present loss of lung function, dyspnea and dry cough. Diagnosis requires compatible radiologic imaging and, in undetermined cases, invasive procedures such as bronchoscopy and surgical lung biopsy. The pathophysiological mechanisms of IPF are not completely understood. Lung injury with abnormal alveolar epithelial repair is thought to be a major cause for activation of profibrotic pathways in IPF...
January 10, 2018: Respiratory Research
https://www.readbyqxmd.com/read/29229270/intratracheal-instillation-of-alveolar-type-ii-cells-enhances-recovery-from-acute-lung-injury-in-rats
#15
Raquel Guillamat-Prats, Ferranda Puig, Marta Camprubí-Rimblas, Raquel Herrero, Anna Serrano-Mollar, Maria Nieves Gómez, Jessica Tijero, Michael A Matthay, Lluís Blanch, Antonio Artigas
BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by excess production of inflammatory factors. Alveolar type II (ATII) cells help repair damaged lung tissue, rapidly proliferating and differentiating into alveolar type I cells after epithelial cell injury. In ALI, the lack of viable ATII favors progression to more severe lung injury. ATII cells regulate the immune response by synthesizing surfactant and other anti-inflammatory proteins and lipids...
November 8, 2017: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/29206808/extrinsic-calcitonin-gene-related-peptide-inhibits-hyperoxia-induced-alveolar-epithelial-type-ii-cells-apoptosis-oxidative-stress-and-reactive-oxygen-species-ros-production-by-enhancing-notch-1-and-homocysteine-induced-endoplasmic-reticulum-protein-herp-expression
#16
Yu-Xin Bai, Fang Fang, Jia-Ling Jiang, Feng Xu
BACKGROUND Lung alveolar epithelial type II cells (AEC II) are the most important stem cells in lung tissues, which are critical for wound repair of bronchopulmonary dysplasia (BPD). This study investigated the effects of calcitonin gene-related peptide (CGRP) on AEC II cells exposed to hyperoxia. MATERIAL AND METHODS Neonatal rat AEC II cells were isolated and identified by detecting surfactant protein C (SP-C). Three small interfering RNAs targeting Notch 1 were synthesized and transfected into AEC II. A hyperoxia-exposed AEC II cell injury model was established and was divided into 8 groups...
December 5, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29163456/mir-194-inhibits-innate-antiviral-immunity-by-targeting-fgf2-in-influenza-h1n1-virus-infection
#17
Keyu Wang, Chengcai Lai, Hongjing Gu, Lingna Zhao, Min Xia, Penghui Yang, Xiliang Wang
Fibroblast growth factor 2 (FGF2 or basic FGF) regulates a wide range of cell biological functions including proliferation, angiogenesis, migration, differentiation, and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza A virus (IAV)-induced lung injury remain largely unexplored. In this study, we report that microRNA-194-5p (miR-194) expression is significantly decreased in A549 alveolar epithelial cells (AECs) following infection with IAV/Beijing/501/2009 (BJ501)...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/29111769/xeroderma-pigmentosum-group-c-deficiency-alters-cigarette-smoke-dna-damage-cell-fate-and-accelerates-emphysema-development
#18
Catherine R Sears, Huaxin Zhou, Matthew J Justice, Amanda J Fisher, Jacob Saliba, Isaac Lamb, Jessica Wicker, Kelly S Schweitzer, Irina Petrache
Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but are thought to involve persistent cytotoxic or mutagenic DNA damage induced by CS. Using complementary cell culture and mouse models of CS exposure, we investigated the role of the DNA repair protein, xeroderma pigmentosum group C (XPC), on CS-induced DNA damage repair and emphysema...
March 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29083412/resolvind-1-stimulates-epithelial-wound-repair-and-inhibits-tgf-%C3%AE-induced-emt-whilst-reducing-fibroproliferation-and-collagen-production
#19
Shengxing Zheng, Qian Wang, Vijay D'Souza, Dom Bartis, Rachel Dancer, Dhruv Parekh, Fang Gao, Qingquan Lian, Shengwei Jin, David R Thickett
Acute and chronic inflammatory lung diseases are often associated with epithelial cell injury/loss and fibroproliferative responses. ResolvinD1 (RvD1) is biosynthesized during the resolution phase of inflammatory response and exerts potent anti-inflammatory and promotes resolution of inflammatory lung diseases. The aim of this study was to investigate whether RvD1 exerts protective effects on alveolar epithelial cell function/differentiation and protects against fibroproliferative stimuli. Primary human alveolar type II cells were used to model the effects of RvD1 in vitro upon wound repair, proliferation, apoptosis, transdifferentiation, and epithelial-mesenchymal transition (EMT)...
January 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29056548/human-induced-pluripotent-stem-cell-derived-lung-progenitor-and-alveolar-epithelial-cells-attenuate-hyperoxia-induced-lung-injury
#20
Mehdi Shafa, Lavinia Iuliana Ionescu, Arul Vadivel, Jennifer J P Collins, Liqun Xu, Shumei Zhong, Martin Kang, Geneviève de Caen, Manijeh Daneshmand, Jenny Shi, Katherine Z Fu, Andrew Qi, Ying Wang, James Ellis, William L Stanford, Bernard Thébaud
BACKGROUND AIMS: Bronchopulmonary dysplasia (BPD), a chronic lung disease characterized by disrupted lung growth, is the most common complication in extreme premature infants. BPD leads to persistent pulmonary disease later in life. Alveolar epithelial type 2 cells (AEC2s), a subset of which represent distal lung progenitor cells (LPCs), promote normal lung growth and repair. AEC2 depletion may contribute to persistent lung injury in BPD. We hypothesized that induced pluripotent stem cell (iPSC)-derived AECs prevent lung damage in experimental oxygen-induced BPD...
January 2018: Cytotherapy
keyword
keyword
84772
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"