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Mouse emphysema

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https://www.readbyqxmd.com/read/29453277/editing-out-five-serpina1-paralogs-to-create-a-mouse-model-of-genetic-emphysema
#1
Florie Borel, Huaming Sun, Marina Zieger, Andrew Cox, Brynn Cardozo, Weiying Li, Gabriella Oliveira, Airiel Davis, Alisha Gruntman, Terence R Flotte, Michael H Brodsky, Andrew M Hoffman, Mai K Elmallah, Christian Mueller
Chronic obstructive pulmonary disease affects 10% of the worldwide population, and the leading genetic cause is α-1 antitrypsin (AAT) deficiency. Due to the complexity of the murine locus, which includes up to six Serpina1 paralogs, no genetic animal model of the disease has been successfully generated until now. Here we create a quintuple Serpina1a-e knockout using CRISPR/Cas9-mediated genome editing. The phenotype recapitulates the human disease phenotype, i.e., absence of hepatic and circulating AAT translates functionally to a reduced capacity to inhibit neutrophil elastase...
February 16, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29447461/genetic-ablation-of-p16-ink4a-does-not-protect-against-cellular-senescence-in-mouse-models-of-copd-emphysema
#2
Isaac K Sundar, Kahkashan Rashid, Janice Gerloff, Dongmei Li, Irfan Rahman
Cigarette smoke (CS) affects DNA damage and cellular senescence signaling pathways in the pathogenesis of chronic obstructive pulmonary disease (COPD). p16(INK4a) (p16: a cyclin-dependent kinase inhibitor) is a key marker of cellular senescence, which is induced by CS in lung cells. It is thought that removal of p16 attenuates premature aging by removing senesced cells. However, the role of p16 in CS-induced stress induce premature senescence (SIPS) and senescence-associated secretory phenotype (SASP during the development of COPD/emphysema is not known...
February 15, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29438939/at-rvd1-repairs-mouse-lung-after-cigarette-smoke-induced-emphysema-via-downregulation-of-oxidative-stress-by-nrf2-keap1-pathway
#3
Sara Vergel Posso, Nicolas Quesnot, João Alfredo Moraes, Lycia Brito-Gitirana, Emanuel Kennedy-Feitosa, Marina Valente Barroso, Luís Cristóvão Porto, Manuella Lanzetti, Samuel Santos Valença
Long-term exposure to cigarette smoke (CS) results in alveolar parenchyma destruction due to chronic inflammatory response and the imbalance between oxidants and antioxidants, and proteases and antiproteases. Emphysema is the main symptom of chronic obstructive pulmonary disease. Current treatment focuses on relieving respiratory symptoms, and inflammation resolution failure is an important pathophysiological element of the disease. Specialized pro-resolving mediators (SPMs) synthesized endogenously during resolution processes demonstrated beneficial effects in murine models of airway inflammation...
February 10, 2018: International Immunopharmacology
https://www.readbyqxmd.com/read/29428733/mice-overexpressing-latent-matrix-metalloproteinase-2-develop-lung-emphysema-after-short-term-exposure-to-cigarette-smoke-extract
#4
Masahiro Onishi, Tetsu Kobayashi, Corina N D'Alessandro-Gabazza, Hajime Fujimoto, Ayshwarya-Lakshmi Chelakkot-Govindalayathil, Yoshinori Takahashi, Taro Yasuma, Kota Nishihama, Masaaki Toda, Yoshiyuki Takei, Osamu Taguchi, Esteban C Gabazza
Chronic obstructive pulmonary disease is the major growing cause of mortality and morbidity worldwide, and it is going to become the third most common cause of death by 2020. Chronic obstructive pulmonary disease is pathologically characterized by lung emphysema and small airway inflammation. Animal models are very important to get insights into the disease pathogenesis but current models of chronic obstructive pulmonary disease take a long time to develop. The need of a new model is compelling. In the present study we focus on the role of matrix metalloproteinases in the pathogenesis of chronic obstructive pulmonary disease and hypothesized that lung overexpression of latent matrix metalloproteinases-2 would allow the development of emphysema after short-term exposure to cigarette smoke extract inhalation...
February 8, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29420065/role-for-cela1-in-postnatal-lung-remodeling-and-aat-deficient-emphysema
#5
Rashika Joshi, Andrea Heinz, Qiang Fan, Shuling Guo, Brett Monia, Christian E H Schmelzer, Anthony S Weiss, Matthew Batie, Harikrishnan Parameshwaran, Brian M Varisco
RATIONALE: α1-antitrypsin (AAT) deficiency-related emphysema is the fourth leading indication for lung transplantation. Chymotrypsin-like elastase 1 (Cela1) is a digestive protease that is expressed during lung development in association with regions of elastin remodeling, exhibits stretch-dependent expression during lung regeneration, and binds lung elastin in a stretch-dependent manner. AAT covalently neutralizes Cela1 in vitro. OBJECTIVES: We sought to determine the role of Cela1 in postnatal lung physiology, whether it interacted with AAT in vivo, and any effects it may have in the context of AAT deficiency...
February 8, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29406250/matrix-metalloproteinases-in-emphysema
#6
REVIEW
Sina A Gharib, Anne M Manicone, William C Parks
Several studies have implicated a causative role for specific matrix metalloproteinases (MMPs) in the development and progression of cigarette smoke-induced chronic obstructive pulmonary disease (COPD) and its severe sequela, emphysema. However, the precise function of any given MMP in emphysema remains an unanswered question. Emphysema results from the degradation of alveolar elastin - among other possible mechanisms - a process that is often thought to be caused by elastolytic proteinases made by macrophages...
January 30, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29381718/effects-of-long-term-cigarette-smoke-exposure-on-bone-metabolism-structure-and-quality-in-a-mouse-model-of-emphysema
#7
Mamoru Sasaki, Shotaro Chubachi, Naofumi Kameyama, Minako Sato, Mizuha Haraguchi, Masaki Miyazaki, Saeko Takahashi, Takayoshi Nakano, Yukiko Kuroda, Tomoko Betsuyaku, Koichi Matsuo
Smoking is a common risk factor for both chronic obstructive pulmonary disease (COPD) and osteoporosis. In patients with COPD, severe emphysema is a risk factor for vertebral fracture; however, the effects of smoking or emphysema on bone health remain largely unknown. We report bone deterioration in a mouse model of emphysema induced by nose-only cigarette smoke (CS) exposure. Unexpectedly, short-term exposure for 4-weeks decreased bone turnover and increased bone volume in mice. However, prolonged exposure for 20- and 40-weeks reversed the effects from suppression to promotion of bone resorption...
2018: PloS One
https://www.readbyqxmd.com/read/29368450/frequency-dependent-airway-hyperresponsiveness-in-a-mouse-model-of-emphysema-and-allergic-inflammation
#8
Kentaro Tamura, Koichiro Matsumoto, Satoru Fukuyama, Keiko Kan-O, Yumiko Ishii, Ken Tonai, Miyoko Tatsuta, Aimi Enokizu, Hiromasa Inoue, Yoichi Nakanishi
Asthma and chronic obstructive pulmonary disease (COPD), chronic airway inflammatory diseases characterized by airflow limitation, have different etiologies and pathophysiologies. Asthma-COPD Overlap (ACO) has recently been used for patients with mixed asthma and COPD. The pathophysiological mechanisms of ACO have not been clearly understood due to the lack of an appropriate murine model. To investigate its pathophysiology, we examined a murine model by allergen challenge in surfactant protein-D (SP-D)-deficient mice that spontaneously developed pulmonary emphysema...
January 2018: Physiological Reports
https://www.readbyqxmd.com/read/29355504/parp-1-inhibition-ameliorates-elastase-induced-lung-inflammation-and-emphysema-in-mice
#9
Vivek Dharwal, Amarjit S Naura
COPD is associated with high morbidity and mortality and no effective treatment is available till date. We have previously reported that PARP-1 plays an important role in the establishment of airway inflammation associated with asthma and ALI. In the present work, we have evaluated the beneficial effects of PARP-1 inhibition on COPD pathogenesis utilizing elastase induced mouse model of the disease. Our data show that PARP-1 inhibition by olaparib significantly reduced the elastase-induced recruitment of inflammatory cells particularly neutrophils in the lungs of mice when administered at dose of 5mg/kg b...
January 17, 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29314863/bacterial-derived-neutrophilic-inflammation-drives-lung-remodeling-in-a-mouse-model-of-copd
#10
Bradley W Richmond, Rui-Hong Du, Wei Han, John T Benjamin, Riet van der Meer, Linda Gleaves, Marshall Guo, Austin McKissack, Yongqin Zhang, Dong-Sheng Cheng, Vasiliy V Polosukhin, Timothy S Blackwell
Loss of secretory immunoglobulin A (SIgA) is common in the small airways of patients with chronic obstructive pulmonary disease (COPD) and may contribute to disease pathogenesis. Using mice that lack SIgA in the airways due to genetic deficiency of polymeric immunoglobulin receptor (pIgR-/- mice), we investigated the role of neutrophils in driving the fibrotic small airway wall remodeling and emphysema that develops spontaneously in these mice. By flow cytometry, we found an increase in the percentage of neutrophils among CD45+ cells in the lungs, as well as an increase in total neutrophils, in pIgR-/- mice compared to wild-type (WT) controls...
January 9, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29138553/the-protective-effect-of-prmt6-overexpression-on-cigarette-smoke-extract-induced-murine-emphysema-model
#11
Xue He, Tiao Li, Naixin Kang, Huihui Zeng, Siying Ren, Dandan Zong, Jinhua Li, Shan Cai, Ping Chen, Yan Chen
Background: Cigarette smoke exposure is the most common risk factor for emphysema, which is one of the major pathologies of COPD. Protein arginine methyltransferase 6 (PRMT6) is a nuclear enzyme that specially catalyzes dimethylation of R2 in histone H3 (H3R2me2a). H3R2me2a prevents trimethylation of H3K4 (H3K4me3), which is located in the transcription start sites of genes in mammalian genomes. We attempted to determine the expression of PRMT6 in human samples, and investigate whether the upregulation of PRMT6 expression can attenuate the development of cigarette smoke extract (CSE)-induced emphysema...
2017: International Journal of Chronic Obstructive Pulmonary Disease
https://www.readbyqxmd.com/read/29137224/role-of-the-inflammasome-in-chronic-obstructive-pulmonary-disease-copd
#12
Chiara Colarusso, Michela Terlizzi, Antonio Molino, Aldo Pinto, Rosalinda Sorrentino
Inflammation is central to the development of chronic obstructive pulmonary disease (COPD), a pulmonary disorder characterized by chronic bronchitis, chronic airway obstruction, emphysema, associated to progressive and irreversible decline of lung function. Emerging genetic and pharmacological evidence suggests that IL-1-like cytokines are highly detected in the sputum and broncho-alveolar lavage (BAL) of COPD patients, implying the involvement of the multiprotein complex inflammasome. So far, scientific evidence has focused on nucleotide-binding oligomerization domain-like receptors protein 3 (NLRP3) inflammasome, a specialized inflammatory signaling platform that governs the maturation and secretion of IL-1-like cytokines through the regulation of caspase-1-dependent proteolytic processing...
October 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29133847/female-mice-lacking-pald1-exhibit-endothelial-cell-apoptosis-and-emphysema
#13
Isabel Egaña, Hiroshi Kaito, Anja Nitzsche, Lore Becker, Carolina Ballester-Lopez, Colin Niaudet, Milena Petkova, Wei Liu, Michael Vanlandewijck, Alexandra Vernaleken, Thomas Klopstock, Helmut Fuchs, Valerie Gailus-Durner, Martin Hrabe de Angelis, Helge Rask-Andersen, Henrik J Johansson, Janne Lehtiö, Liqun He, Ali Ö Yildirim, Mats Hellström
Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype...
November 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29127016/enhanced-activation-of-circulating-plasmacytoid-dendritic-cells-in-patients-with-chronic-obstructive-pulmonary-disease-and-experimental-smoking-induced-emphysema
#14
Shi-Lin Qiu, Liang-Jian Kuang, Qi-Ya Tang, Min-Chao Duan, Jing Bai, Zhi-Yi He, Jian-Quan Zhang, Mei-Hua Li, Jing-Min Deng, Guang-Nan Liu, Xiao-Ning Zhong
Plasmacytoid dendritic cells (pDCs) are key cells bridging the innate with adaptive immunity. However, the phenotypic characteristics of circulating pDCs and its role in smoking related-Chronic Obstructive Pulmonary Disease (COPD) remain largely unknown. The aim of this study was analyzed the phenotype of circulating pDCs and the expression of IFN-γ producing CD8(+)T cells and IL-17-producing CD8(+)T cells in patients with COPD by using multi-colour flow cytometry. The cytokine profiles in peripheral blood from all subjects were measured by ELISA...
November 7, 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/29111769/xpc-deficiency-alters-cigarette-smoke-dna-damage-cell-fate-and-accelerates-emphysema-development
#15
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...
November 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29100513/ghrelin-therapy-improves-lung-and-cardiovascular-function-in-experimental-emphysema
#16
Nazareth de Novaes Rocha, Milena Vasconcellos de Oliveira, Cássia Lisboa Braga, Gabriela Guimarães, Lígia de Albuquerque Maia, Gisele de Araújo Padilha, Johnatas Dutra Silva, Christina Maeda Takiya, Vera Luiza Capelozzi, Pedro Leme Silva, Patricia Rieken Macedo Rocco
BACKGROUND: Emphysema is a progressive disease characterized by irreversible airspace enlargement followed by a decline in lung function. It also causes extrapulmonary effects, such as loss of body mass and cor pulmonale, which are associated with shorter survival and worse clinical outcomes. Ghrelin, a growth-hormone secretagogue, stimulates muscle anabolism, has anti-inflammatory effects, promotes vasodilation, and improves cardiac performance. Therefore, we hypothesized that ghrelin might reduce lung inflammation and remodelling as well as improve lung mechanics and cardiac function in experimental emphysema...
November 3, 2017: Respiratory Research
https://www.readbyqxmd.com/read/29100417/inhibition-of-endoplasmic-reticulum-stress-alleviates-cigarette-smoke-induced-airway-inflammation-and-emphysema
#17
Yong Wang, Zhen-Zhen Wu, Wei Wang
Chronic bronchitis and emphysema are pathologic features of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS)-induced endoplasmic reticulum (ER) stress has been implicated in the COPD development, but the molecular mechanism by which it contributes to COPD etiology and the specific role it plays in COPD pathogenesis remain poorly understood. Here, we aimed to determine the role of ER stress in the pathogenesis of CS-induced airway inflammation and emphysema. Exposure to CS significantly increased the expression of ER stress markers in Beas-2B cells and in mouse lungs, possibly through the production of oxidative stress...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29078374/taurine-ameliorates-particulate-matter-induced-emphysema-by-switching-on-mitochondrial-nadh-dehydrogenase-genes
#18
Xiaobo Li, Hongbao Yang, Hao Sun, Runze Lu, Chengcheng Zhang, Na Gao, Qingtao Meng, Shenshen Wu, Susanna Wang, Michael Aschner, Jiong Wu, Boping Tang, Aihua Gu, Steve A Kay, Rui Chen
Chronic obstructive pulmonary disease (COPD) has been linked to particulate matter (PM) exposure. Using transcriptomic analysis, we demonstrate that diesel exhaust particles, one of the major sources of particulate emission, down-regulated genes located in mitochondrial complexes I and V and induced experimental COPD in a mouse model. 1-Nitropyrene was identified as a major toxic component of PM-induced COPD. In the panel study, COPD patients were found to be more susceptible to PM than individuals with normal lung function due to an increased inflammatory response...
November 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29038519/resveratrol-therapeutics-combines-both-antimicrobial-and-immunomodulatory-properties-against-respiratory-infection-by-nontypeable-haemophilus-influenzae
#19
Begoña Euba, Nahikari López-López, Irene Rodríguez-Arce, Ariadna Fernández-Calvet, Montserrat Barberán, Nuria Caturla, Sara Martí, Roberto Díez-Martínez, Junkal Garmendia
The respiratory pathogen nontypeable Haemophilus influenzae (NTHi) is an important cause of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) that requires efficient treatments. A previous screening for host genes differentially expressed upon NTHi infection identified sirtuin-1, which encodes a NAD-dependent deacetylase protective against emphysema and is activated by resveratrol. This polyphenol concomitantly reduces NTHi viability, therefore highlighting its therapeutic potential against NTHi infection at the COPD airway...
October 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29019171/optimization-of-culture-conditions-for-rapid-clinical-scale-expansion-of-human-umbilical-cord-blood-derived-mesenchymal-stem-cells
#20
Wankyu Choi, Soon-Jae Kwon, Hye Jin Jin, Sang Young Jeong, Soo Jin Choi, Wonil Oh, Yoon Sun Yang, Hong Bae Jeon, Eun Su Jeon
BACKGROUND: Mesenchymal stem cells (MSCs) have broad-spectrum therapeutic effects in various diseases, and thus have many clinical applications. However, it is difficult to produce sufficient numbers of MSCs for clinical use, and improved culture systems are required. Here, we report the effects of calcium (Ca(2+)) and hypoxia on the proliferation of human umbilical cord blood-derived MSCs (hUCB-MSCs). In addition, we determined the optimal conditions of these two factors for the large-scale culture of hUCB-MSCs...
October 10, 2017: Clinical and Translational Medicine
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