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Mouse emphysema

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https://www.readbyqxmd.com/read/28399390/matrix-metalloproteinase-28-is-a-key-contributor-to-emphysema-pathogenesis
#1
Anne M Manicone, Sina A Gharib, Ke-Qin Gong, William E Eddy, Matthew E Long, Charles W Frevert, William A Altemeier, William C Parks, A McGarry Houghton
Chronic obstructive pulmonary disease (COPD) comprises chronic bronchitis and emphysema, and is a leading cause of morbidity and mortality. Because tissue destruction is the prominent characteristic of emphysema, extracellular proteinases, particularly those with elastolytic ability, are often considered to be key drivers in this disease. Several human and mouse studies have implicated roles for matrix metalloproteinases (MMPs), particularly macrophage-derived proteinases, in COPD pathogenesis. MMP-28 is expressed by the pulmonary epithelium and macrophage, and we have found that it regulates macrophage recruitment and polarization...
April 8, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28315337/p53-signaling-pathway-polymorphisms-associated-with-emphysematous-changes-in-copd-patients
#2
Shiro Mizuno, Takeshi Ishizaki, Maiko Kadowaki, Masaya Akai, Kohei Shiozaki, Masaharu Iguchi, Taku Oikawa, Ken Nakagawa, Kazuhiro Osanai, Hirohisa Toga, Jose Gomez-Arroyo, Donatas Kraskauskas, Carlyne D Cool, Herman J Bogaard, Norbert F Voelkel
BACKGROUND: The p53 signaling pathway may be important for the pathogenesis of emphysematous changes in the lungs of smokers. Polymorphism of p53 at codon 72 is known to affect apoptotic effector proteins, and the polymorphism of mouse double minute 2 homolog (MDM2) SNP309 is known to increase MDM2 expression. The aim of this study was to assess polymorphisms of the p53 and MDM2 genes in smokers and confirm the role of SNPs in these genes in the pathogenesis of pulmonary emphysema. METHODS: 365 patients with a smoking history were included in this study, and the polymorphisms of p53 and MDM2 genes were identified...
March 14, 2017: Chest
https://www.readbyqxmd.com/read/28287180/functional-interactors-of-three-genome-wide-association-study-genes-are-differentially-expressed-in-severe-chronic-obstructive-pulmonary-disease-lung-tissue
#3
Jarrett D Morrow, Xiaobo Zhou, Taotao Lao, Zhiqiang Jiang, Dawn L DeMeo, Michael H Cho, Weiliang Qiu, Suzanne Cloonan, Victor Pinto-Plata, Bartholome Celli, Nathaniel Marchetti, Gerard J Criner, Raphael Bueno, George R Washko, Kimberly Glass, John Quackenbush, Augustine M K Choi, Edwin K Silverman, Craig P Hersh
In comparison to genome-wide association studies (GWAS), there has been poor replication of gene expression studies in chronic obstructive pulmonary disease (COPD). We performed microarray gene expression profiling on a large sample of resected lung tissues from subjects with severe COPD. Comparing 111 COPD cases and 40 control smokers, 204 genes were differentially expressed; none were at significant GWAS loci. The top differentially expressed gene was HMGB1, which interacts with AGER, a known COPD GWAS gene...
March 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28273689/progranulin-protects-lung-epithelial-cells-from-cigarette-smoking-induced-apoptosis
#4
Kyoung Young Lee, So-Young Park, Sunjoo Park, Gyong Hwa Hong, Keun-Ai Moon, You-Sun Kim, Yeon-Mok Oh, Hyouk-Soo Kwon, Tae-Bum Kim, Hee-Bom Moon, You Sook Cho
BACKGROUND AND OBJECTIVE: Emphysema is characterized by irreversible destruction of alveolar walls with distal air space enlargement. Cigarette smoke (CS) is considered a major risk factor for emphysematous changes in COPD. Progranulin (PGRN), a glycoprotein induced by CS, has been reported to participate in apoptosis. However, the precise role of PGRN in emphysema is currently unknown. This study aimed to evaluate the role of PGRN in human alveolar epithelial cells (AECs) in response to CS...
March 8, 2017: Respirology: Official Journal of the Asian Pacific Society of Respirology
https://www.readbyqxmd.com/read/28252045/latent-tgf-%C3%AE-binding-protein-2-and-4-have-essential-overlapping-functions-in-microfibril-development
#5
Yusuke Fujikawa, Hideyuki Yoshida, Tadashi Inoue, Tetsuya Ohbayashi, Kazuo Noda, Harald von Melchner, Toshiji Iwasaka, Ichiro Shiojima, Tomoya O Akama, Tomoyuki Nakamura
Microfibrils are exracellular matrix components necessary for elastic fiber assembly and for suspending lenses. We previously reported that latent TGF-β binding protein 2 (LTBP-2), a microfibril-associated protein, is required for forming stable microfibril bundles in ciliary zonules. However, it was not understood why Ltbp2 null mice only showed an eye-specific phenotype, whereas LTBP-2 is abundantly expressed in other tissues containing microfibrils in wild type mice. Here, we show that LTBP-4, another microfibril-associated protein, compensates for the loss of LTBP-2 in microfibril formation...
March 2, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28251446/atorvastatin-and-simvastatin-promoted-mouse-lung-repair-after-cigarette-smoke-induced-emphysema
#6
Vanessa Pinho-Ribeiro, Adriana Correa Melo, Emanuel Kennedy-Feitosa, Adriane Graca-Reis, Marina Valente Barroso, Isabella Cattani-Cavalieri, Giovanna Marcella Cavalcante Carvalho, Walter Araújo Zin, Luis Cristóvão Porto, Lycia Brito Gitirana, Manuella Lanzetti, Samuel Santos Valença
Cigarette smoke (CS) induces pulmonary emphysema by inflammation, oxidative stress, and metalloproteinase (MMP) activation. Pharmacological research studies have not focused on tissue repair after the establishment of emphysema but have instead focused on inflammatory stimulation. The aim of our study was to analyze the effects of atorvastatin and simvastatin on mouse lung repair after emphysema caused by CS. Male mice (C57BL/6, n = 45) were divided into the following groups: control (sham-exposed), CSr (mice exposed to 12 cigarettes a day for 60 days and then treated for another 60 days with the vehicle), CSr+A (CSr mice treated with atorvastatin for 60 days), and CSr+S (CSr mice treated with simvastatin for 60 days)...
March 1, 2017: Inflammation
https://www.readbyqxmd.com/read/28248572/transcriptomic-analysis-of-lung-tissue-from-cigarette-smoke-induced-emphysema-murine-models-and-human-copd-show-shared-and-distinct-pathways
#7
Jeong H Yun, Jarrett Morrow, Caroline A Owen, Weiliang Qiu, Kimberly Glass, Taotao Lao, Zhiqiang Jiang, Mark A Perrella, Edwin K Silverman, Xiaobo Zhou, Craig P Hersh
Although cigarette smoke (CS) is the primary risk factor for chronic obstructive pulmonary disease (COPD), the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6, NZW/LacJ) and two genetic models with mutations in COPD genome-wide association study (GWAS) genes (HHIP, FAM13A) after six months of chronic CS exposure and compared the results to human COPD lung tissues...
March 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28237967/heterozygous-vangl2-looptail-mice-reveal-novel-roles-for-the-planar-cell-polarity-pathway-in-adult-lung-homeostasis-and-repair
#8
Thanushiyan Poobalasingam, Laura L Yates, Simone A Walker, Miguel Pereira, Nina Y Gross, Akmol Ali, Maria Kolatsi-Joannou, Marjo-Riitta Jarvelin, Juha Pekkanen, Eugenia Papakrivopoulou, David A Long, Mark Griffiths, Darcy Wagner, Melanie Königshoff, Matthew Hind, Cosetta Minelli, Clare M Lloyd, Charlotte H Dean
Lung diseases impose a huge economic and health burden worldwide. A key aspect of several adult lung diseases, such as idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD), including emphysema, is aberrant tissue repair, which leads to an accumulation of damage and impaired respiratory function. Currently, there are few effective treatments available for these diseases and their incidence is rising. The planar cell polarity (PCP) pathway is critical for the embryonic development of many organs, including kidney and lung...
April 1, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28186975/amp-activated-protein-kinase-reduces-inflammatory-responses-and-cellular-senescence-in-pulmonary-emphysema
#9
Xiao-Yu Cheng, Yang-Yang Li, Cheng Huang, Jun Li, Hong-Wei Yao
Current drug therapy fails to reduce lung destruction of chronic obstructive pulmonary disease (COPD). AMP-activated protein kinase (AMPK) has emerged as an important integrator of signals that control energy balance and lipid metabolism. However, there are no studies regarding the role of AMPK in reducing inflammatory responses and cellular senescence during the development of emphysema. Therefore, we hypothesize that AMPK reduces inflammatroy responses, senescence, and lung injury. To test this hypothesis, human bronchial epithelial cells (BEAS-2B) and small airway epithelial cells (SAECs) were treated with cigarette smoke extract (CSE) in the presence of a specific AMPK activator (AICAR, 1 mM) and inhibitor (Compound C, 5 μM)...
April 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28183199/recombinant-human-keratinocyte-growth-factor-attenuates-apoptosis-in-elastase-induced-emphysematous-mice-lungs
#10
Sudhir Kotnala, Sumit Baghel, Deepali Verma, Amit Tyagi, Jai Prakash Muyal
Alveolar cell apoptosis is one of the potential factors involved in the pathogenesis of emphysema. Recently, exogenous recombinant human keratinocyte growth factor (rHuKGF) has been reported to induce the regeneration of gas exchange structures. Therefore, the rationale of the present study was to investigate the potential effect of rHuKGF in ameliorating tissue destruction in the emphysematous mice lungs. Four experimental groups (i.e. control-, emphysema-, therapy- and therapy control-group) were prepared...
January 2017: Inhalation Toxicology
https://www.readbyqxmd.com/read/28164246/immune-mediated-inflammation-in-the-pathogenesis-of-emphysema-insights-from-mouse-models
#11
REVIEW
John M Craig, Alan L Scott, Wayne Mitzner
The cellular mechanisms that result in the initiation and progression of emphysema are clearly complex. A growing body of human data combined with discoveries from mouse models utilizing cigarette smoke exposure or protease administration have improved our understanding of emphysema development by implicating specific cell types that may be important for the pathophysiology of chronic obstructive pulmonary disease. The most important aspects of emphysematous damage appear to be oxidative or protease stress and sustained macrophage activation and infiltration of other immune cells leading to epithelial damage and cell death...
March 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/28154254/effects-of-simvastatin-on-alveolar-regeneration-and-its-relationship-to-exposure-in-mice-with-dexamethasone-induced-emphysema
#12
Shihomi Hirooka, Misaki Ueno, Satoko Fukuda, Atsushi Miyajima, Takashi Hirota
In the present study, the relationship between systemic exposure of simvastatin (SV) hydroxy acid (SV-acid), an active form of SV, and its alveolar regeneration rates was investigated using emphysema model mice created by postnatal treatment of dexamethasone. In a model with young animals, the mice were treated with SV for 10 d from postnatal day 42. Similar alveolar regeneration with a % mean linear intercept (Lm) recovery of 60 to 70% by histochemical observation was observed in mice after intraperitoneal administration at dose in the range of 4-100 µg/mouse...
2017: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28070015/inhaled-resveratrol-treatments-slow-ageing-related-degenerative-changes-in-mouse-lung
#13
Sonia Navarro, Raghava Reddy, Jooeun Lee, David Warburton, Barbara Driscoll
BACKGROUND: Lung ageing, a significant risk factor for chronic human lung diseases such as COPD and emphysema, is characterised by airspace enlargement and decreasing lung function. Likewise, in prematurely ageing telomerase null (terc-/-) mice, p53 stabilisation within diminishing numbers of alveolar epithelial type 2 cells (AEC2) accompanies reduced lung function. Resveratrol (RSL) is a plant phytoalexin that has previously showed efficacy in enhancing invertebrate longevity and supporting mammalian muscle metabolism when delivered orally...
January 9, 2017: Thorax
https://www.readbyqxmd.com/read/28064485/astragalin-inhibits-allergic-inflammation-and-airway-thickening-in-ovalbumin-challenged-mice
#14
Yun-Ho Kim, Yean-Jung Choi, Min-Kyung Kang, Sin-Hye Park, Lucia Dwi Antika, Eun-Jung Lee, Dong Yeon Kim, Young-Hee Kang
Lung inflammation and oxidative stress are the major contributors to the development of obstructive pulmonary diseases. Macrophages are involved in pulmonary inflammation and alveolar damage in emphysema. Astragalin is an anti-inflammatory flavonoid present in persimmon leaves and green tea seeds. This study elucidated that astragalin inhibited inflammatory cell infiltration induced by 20 μM H2O2 and blocked airway thickening and alveolar emphysema induced by 20 μg of ovalbumin (OVA) in mice. OVA induced mouse pulmonary MCP-1, and H2O2 enhanced the expression of MCP-1/ICAM-1/αv integrin in bronchial airway epithelial BEAS-2B cells...
February 1, 2017: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/28056498/bone-marrow-stem-cell-therapy-partially-ameliorates-pathological-consequences-in-livers-of-mice-expressing-mutant-human-%C3%AE-1-antitrypsin
#15
Prakash Baligar, Veena Kochat, Shailendra K Arindkar, Zaffar Equbal, Snehashish Mukherjee, Swati Patel, Perumal Nagarajan, Sujata Mohanty, Jeffrey H Teckman, Asok Mukhopadhyay
Alpha-1-antitrypsin (AAT) deficiency (AATD) is a genetic disease, caused by mutation of the AAT gene. Accumulation of mutated AAT protein aggregates in hepatocytes leads to endoplasmic reticulum stress, resulting in impairment of liver functions and, in some cases, hepatocellular carcinoma, whereas decline of AAT levels in sera is responsible for pulmonary emphysema. In advanced liver disease, the only option for treatment is liver transplantation, whereas AAT replacement therapy is therapeutic for emphysema...
April 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28034695/aberrant-lung-remodeling-in-a-mouse-model-of-surfactant-dysregulation-induced-by-modulation-of-the-abca3-gene
#16
Michael F Beers, Lars Knudsen, Yaniv Tomer, Julian Maronn, Ming Zhao, Matthias Ochs, Surafel Mulugeta
The lipid transporter, ATP binding cassette class A3 (ABCA3), plays a critical role in the biogenesis of alveolar type 2 (AT2) cell lamellar bodies (LBs). A relatively large number of mutations in the ABCA3 gene have been identified in association with diffuse parenchymal lung disease (DPLD), the most common of which is a missense mutation (valine substitution for lysine at residue 292 (ABCA3(E292V))) that leads to functional impairment of the transporter in vitro. The consequences of ABCA3(E292)(V) gene expression in vivo are unknown...
March 2017: Annals of Anatomy, Anatomischer Anzeiger: Official Organ of the Anatomische Gesellschaft
https://www.readbyqxmd.com/read/28005423/cellular-senescence-and-lung-function-during-aging-yin-and-yang
#17
Judith Campisi
Cellular senescence is a cell fate decision and stress response that entails a permanent arrest of cell proliferation coupled to a complex secretory phenotype. Senescent cells increase in number with age in most, if not all, mammalian tissues, including the airways and lungs. They also increase at greater than expected numbers, compared with age-matched controls, at sites of age-related pathologies such as chronic obstructive pulmonary disorder and emphysema. The senescence response is a double-edged sword...
December 2016: Annals of the American Thoracic Society
https://www.readbyqxmd.com/read/27994590/cigarette-smoke-induction-of-interleukin-27-wsx-1-regulates-the-differentiation-of-th1-and-th17-cells-in-a-smoking-mouse-model-of-emphysema
#18
Shi-Lin Qiu, Min-Chao Duan, Yi Liang, Hai-Juan Tang, Guang-Nan Liu, Liang-Ming Zhang, Chao-Mian Yang
IFN-γ-producing CD4(+) T (Th1) cells and IL-17-producing CD4(+) T (Th17) cells play a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the immune regulation between Th1 and Th17 cells remains unclear. Previous studies have demonstrated that interleukin-27 (IL-27)/WSX-1 exerted pro- or anti-inflammatory effects in many acute inflammatory diseases by modulating T cell-mediated immune response, but little was known about its role in chronic inflammatory disease, especially in smoking-related lung diseases...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27982104/pharmacological-and-genetic-reappraisals-of-protease-and-oxidative-stress-pathways-in-a-mouse-model-of-obstructive-lung-diseases
#19
Tsuyoshi Shuto, Shunsuke Kamei, Hirofumi Nohara, Haruka Fujikawa, Yukihiro Tasaki, Takuya Sugahara, Tomomi Ono, Chizuru Matsumoto, Yuki Sakaguchi, Kasumi Maruta, Ryunosuke Nakashima, Taisei Kawakami, Mary Ann Suico, Yoshitaka Kondo, Akihito Ishigami, Toru Takeo, Ken-Ichiro Tanaka, Hiroshi Watanabe, Naomi Nakagata, Kohei Uchimura, Kenichiro Kitamura, Jian-Dong Li, Hirofumi Kai
Protease-antiprotease imbalance and oxidative stress are considered to be major pathophysiological hallmarks of severe obstructive lung diseases including chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF), but limited information is available on their direct roles in the regulation of pulmonary phenotypes. Here, we utilized βENaC-transgenic (Tg) mice, the previously established mouse model of severe obstructive lung diseases, to produce lower-mortality but pathophysiologically highly useful mouse model by backcrossing the original line with C57/BL6J mice...
December 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27958376/high-resolution-short-exposure-small-animal-laboratory-x-ray-phase-contrast-tomography
#20
Daniel H Larsson, William Vågberg, Andre Yaroshenko, Ali Önder Yildirim, Hans M Hertz
X-ray computed tomography of small animals and their organs is an essential tool in basic and preclinical biomedical research. In both phase-contrast and absorption tomography high spatial resolution and short exposure times are of key importance. However, the observable spatial resolutions and achievable exposure times are presently limited by system parameters rather than more fundamental constraints like, e.g., dose. Here we demonstrate laboratory tomography with few-ten μm spatial resolution and few-minute exposure time at an acceptable dose for small-animal imaging, both with absorption contrast and phase contrast...
December 13, 2016: Scientific Reports
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