keyword
MENU ▼
Read by QxMD icon Read
search

Mouse emphysema

keyword
https://www.readbyqxmd.com/read/29899396/lung-cellular-senescence-is-independent-of-aging-in-a-mouse-model-of-copd-emphysema
#1
Kahkashan Rashid, Isaac K Sundar, Janice Gerloff, Dongmei Li, Irfan Rahman
Cigarette smoke (CS) induces lung cellular senescence that plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). How aging influences cellular senescence and other molecular hallmarks, and increases the risk of CS-induced damage remains unknown. We hypothesized that aging-associated changes in lungs worsen the COPD/emphysema by CS exposure. Younger and older groups of C57BL/6J mice were exposed to chronic CS for 6 months with respective age-matched air-exposed controls...
June 13, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29731780/lung-mesenchymal-stem-cells-ameliorate-elastase-induced-damage-in-an-animal-model-of-emphysema
#2
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/29692733/identification-of-mepenzolate-derivatives-with-long-acting-bronchodilatory-activity
#3
Ken-Ichiro Tanaka, Naoki Yamakawa, Yasunobu Yamashita, Teita Asano, Yuki Kanda, Ayaka Takafuji, Masahiro Kawahara, Mitsuko Takenaga, Yoshifumi Fukunishi, Tohru Mizushima
The standard treatment for chronic obstructive pulmonary disease is a combination of anti-inflammatory drugs and bronchodilators. We recently found that mepenzolate bromide ( MP ), an antagonist for human muscarinic M3 receptor (hM3 R), has both anti-inflammatory and short-acting bronchodilatory activities. To obtain MP derivatives with longer-lasting bronchodilatory activity, we synthesized hybrid compounds based on MP and two other muscarinic antagonists with long-acting bronchodilatory activity glycopyrronium bromide ( GC ) and aclidinium bromide ( AD )...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29659176/nrf2-attenuates-inflammatory-response-in-copd-emphysema-crosstalk-with-wnt3a-%C3%AE-catenin-and-ampk-pathways
#4
Wenhui Cui, Zhihui Zhang, Panpan Zhang, Jiao Qu, Cheng Zheng, Xiaoting Mo, Wencheng Zhou, Liang Xu, Hongwei Yao, Jian Gao
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and abnormal inflammatory response. Wnt/β-catenin and AMP-activated protein kinase (AMPK) have been shown to modulate lung inflammatory responses and injury. However, it remains elusive whether Wnt/β-catenin and AMPK modulate nuclear factor erythroid-2 related factor-2 (Nrf2)-mediated protective responses during the development of emphysema. Here we showed that treatment with a Wnt pathway activator (LiCl) reduced elastase-induced airspace enlargement and cigarette smoke extract (CSE)-induced lung inflammatory responses in WT mice, which was associated with increased activation of Nrf2 pathway...
April 16, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29554594/atorvastatin-dose-dependently-promotes-mouse-lung-repair-after-emphysema-induced-by-elastase
#5
Adriana Correa Melo, Isabella Cattani-Cavalieri, Marina Valente Barroso, Nicolas Quesnot, Lycia Brito Gitirana, Manuella Lanzetti, Samuel Santos Valença
Emphysema results in a proteinase - antiproteinase imbalance, inflammation and oxidative stress. Our objective was to investigate whether atorvastatin could repair mouse lungs after elastase-induced emphysema. Vehicle (50 μL) or porcine pancreatic elastase (PPE) was administered on day 1, 3, 5 and 7 at 0.6 U intranasally. Male mice were divided into a control group (sham), PPE 32d (sacrificed 24 h after 32 days), PPE 64d (sacrificed 24 h after 64 days), and atorvastatin 1, 5 and 20 mg treated from day 33 until day 64 and sacrificed 24 h later (A1 mg, A5 mg and A20 mg, respectively)...
June 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29507104/mtor-suppresses-cigarette-smoke-induced-epithelial-cell-death-and-airway-inflammation-in-chronic-obstructive-pulmonary-disease
#6
Yong Wang, Juan Liu, Jie-Sen Zhou, Hua-Qiong Huang, Zhou-Yang Li, Xu-Chen Xu, Tian-Wen Lai, Yue Hu, Hong-Bin Zhou, Hai-Pin Chen, Song-Min Ying, Wen Li, Hua-Hao Shen, Zhi-Hua Chen
Airway epithelial cell death and inflammation are pathological features of chronic obstructive pulmonary disease (COPD). Mechanistic target of rapamycin (MTOR) is involved in inflammation and multiple cellular processes, e.g., autophagy and apoptosis, but little is known about its function in COPD pathogenesis. In this article, we illustrate how MTOR regulates cigarette smoke (CS)-induced cell death, airway inflammation, and emphysema. Expression of MTOR was significantly decreased and its suppressive signaling protein, tuberous sclerosis 2 (TSC2), was increased in the airway epithelium of human COPD and in mouse lungs with chronic CS exposure...
April 15, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29453277/editing-out-five-serpina1-paralogs-to-create-a-mouse-model-of-genetic-emphysema
#7
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...
March 13, 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
#8
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
#9
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...
March 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
#10
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 26, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29420065/role-for-cela1-in-postnatal-lung-remodeling-and-aat-deficient-emphysema
#11
Rashika Joshi, Andrea Heinz, Qiang Fan, Shuling Guo, Brett Monia, Christian E H Schmelzer, Anthony S Weiss, Matthew Batie, Harikrishnan Parameswaran, 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
#12
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...
March 23, 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
#13
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
#14
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
#15
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 a dose of 5 mg/kg b...
April 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29314863/bacterial-derived-neutrophilic-inflammation-drives-lung-remodeling-in-a-mouse-model-of-chronic-obstructive-pulmonary-disease
#16
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 IgA is common in the small airways of patients with chronic obstructive pulmonary disease and may contribute to disease pathogenesis. Using mice that lack secretory IgA in the airways due to genetic deficiency of polymeric Ig 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 with wild-type controls...
June 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
#17
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
#18
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
#19
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
#20
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 8, 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
keyword
keyword
112376
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"