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Bleomycin pulmonary fibrosis

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https://www.readbyqxmd.com/read/28325283/silencing-of-carbohydrate-sulfotransferase-15-hinders-murine-pulmonary-fibrosis-development
#1
Yoshiro Kai, Koichi Tomoda, Hiroyuki Yoneyama, Masahiro Kitabatake, Atsuhiro Nakamura, Toshihiro Ito, Masanori Yoshikawa, Hiroshi Kimura
Pulmonary fibrosis is a progressive lung disorder characterized by interstitial fibrosis, for which no effective treatments are available. Chondroitin sulfate proteoglycan (CSPG) has been shown to be a mediator, but the specific component of glycosaminoglycan chains of CSPG has not been explored. We show that chondroitin sulfate E-type (CS-E) is involved in fibrogenesis. Small interfering RNA (siRNA) targeting carbohydrate sulfotransferase 15 (CHST15) was designed to inhibit CHST15 mRNA and its product, CS-E...
March 17, 2017: Molecular Therapy. Nucleic Acids
https://www.readbyqxmd.com/read/28323056/fty720-promotes-pulmonary-fibrosis-when-administered-during-the-remodelling-phase-following-a-bleomycin-induced-lung-injury
#2
David R Gendron, Anne-Marie Lemay, Pascale Blais Lecours, Valérie Perreault-Vallières, Carole-Ann Huppé, Ynuk Bossé, Marie-Renée Blanchet, Geneviève Dion, David Marsolais
Fibrosis complicates numerous pathologies including interstitial lung diseases. Sphingosine analogs such as FTY720 can alleviate lung injury-induced fibrosis in murine models. Contradictorily, FTY720 also promotes in vitro processes normally leading to fibrosis and high doses in vivo foster lung fibrosis by enhancing vascular leakage into the lung. The goal of this study was to determine the effect of low doses of FTY720 on lung fibrosis triggered by an acute injury in mice. We first defined the time-boundaries delimiting the inflammatory and remodelling phases of an injury elicited by bleomycin based on neutrophil counts, total lung capacity and lung stiffness...
March 16, 2017: Pulmonary Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28320097/asiatic-acid-ameliorates-pulmonary-fibrosis-induced-by-bleomycin-blm-via-suppressing-pro-fibrotic-and-inflammatory-signaling-pathways
#3
Shu-Hong Dong, Yan-Wei Liu, Feng Wei, Hui-Zhen Tan, Zhi-Dong Han
Idiopathic pulmonary fibrosis is known as a life-threatening disease with high mortality and limited therapeutic strategies. In addition, the molecular mechanism by which pulmonary fibrosis developed is not fully understood. Asiatic acid (AA) is a triterpenoid, isolated from Centella asiatica, exhibiting efficient anti-inflammatory and anti-oxidative activities. In our study, we attempted to explore the effect of Asiatic acid on bleomycin (BLM)-induced pulmonary fibrosis in mice. The findings indicated that pre-treatment with Asiatic acid inhibited BLM-induced lung injury and fibrosis progression in mice...
March 17, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28304344/nrf2-regulates-the-risk-of-a-diesel-exhaust-inhalation-induced-immune-response-during-bleomycin-lung-injury-and-fibrosis-in-mice
#4
Ying-Ji Li, Takako Shimizu, Yusuke Shinkai, Yukiyo Hirata, Hirofumi Inagaki, Ken Takeda, Arata Azuma, Masayuki Yamamoto, Tomoyuki Kawada
The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both Nrf2(+/+) and Nrf2(-/-) C57BL/6J mice on day 0. The mice were exposed to DE for 56 days from 28 days before the BLM injection to 28 days after the BLM injection. Inhalation of DE induced significant inhibition of airway clearance function and the proinflammatory cytokine secretion in macrophages, an increase in neutrophils, and severe lung inflammatory injury, which were greater in Nrf2(-/-) mice than in Nrf2(+/+) mice...
March 17, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28300665/grape-seed-extract-ameliorates-bleomycin-induced-mouse-pulmonary-fibrosis
#5
Qi Liu, Jun-Xia Jiang, Ya-Nan Liu, Yan Guan, Wei Zhao, Yong-Liang Jia, Xin-Wei Dong, Yun Sun, Qiang-Min Xie
Pulmonary fibrosis is common in a variety of inflammatory lung diseases, such as interstitial pneumonia, chronic obstructive pulmonary disease, and silicosis. There is currently no effective clinical drug treatment. It has been reported that grape seed extracts (GSE) has extensive pharmacological effects with minimal toxicity. Although it has been found that GSE can improve the lung collagen deposition and fibrosis pathology induced by bleomycin in rat, its effects on pulmonary function, inflammation, growth factors, matrix metalloproteinases and epithelial-mesenchymal transition remain to be researched...
March 11, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28298912/heterologous-matrix-metalloproteinase-gene-promoter-activity-allows-in-vivo-real-time-imaging-of-bleomycin-induced-lung-fibrosis-in-transiently-transgenized-mice
#6
Fabio Franco Stellari, Francesca Ruscitti, Daniela Pompilio, Francesca Ravanetti, Giulia Tebaldi, Francesca Macchi, Andrea Elizabeth Verna, Gino Villetti, Gaetano Donofrio
Idiopathic pulmonary fibrosis is a very common interstitial lung disease derived from chronic inflammatory insults, characterized by massive scar tissue deposition that causes the progressive loss of lung function and subsequent death for respiratory failure. Bleomycin is used as the standard agent to induce experimental pulmonary fibrosis in animal models for the study of its pathogenesis. However, to visualize the establishment of lung fibrosis after treatment, the animal sacrifice is necessary. Thus, the aim of this study was to avoid this limitation by using an innovative approach based on a double bleomycin treatment protocol, along with the in vivo images analysis of bleomycin-treated mice...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28297588/oncostatin-m-preconditioned-mesenchymal-stem-cells-alleviate-bleomycin-induced-pulmonary-fibrosis-through-paracrine-effects-of-the-hepatocyte-growth-factor
#7
Ying-Wei Lan, Si-Min Theng, Tsung-Teng Huang, Kong-Bung Choo, Chuan-Mu Chen, Han-Pin Kuo, Kowit-Yu Chong
Mesenchymal stem cells (MSCs) are widely considered for treatment of pulmonary fibrosis based on the anti-inflammatory, antifibrotic, antiapoptotic, and regenerative properties of the cells. Recently, elevated levels of oncostatin M (OSM) have been reported in the bronchoalveolar lavage fluid of a pulmonary fibrosis animal model and in patients. In this work, we aimed to prolong engrafted MSC survival and to enhance the effectiveness of pulmonary fibrosis transplantation therapy by using OSM-preconditioned MSCs...
March 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28292882/cthrc1-lowers-pulmonary-collagen-associated-with-bleomycin-induced-fibrosis-and-protects-lung-function
#8
Andrew P Binks, Megyn Beyer, Ryan Miller, Renee J LeClair
Idiopathic pulmonary fibrosis (IPF) involves collagen deposition that results in a progressive decline in lung function. This process involves activation of Smad2/3 by transforming growth factor (TGF)-β and Wnt signaling pathways. Collagen Triple Helix Repeat-Containing-1 (Cthrc1) protein inhibits Smad2/3 activation. To test the hypothesis that Cthrc1 limits collagen deposition and the decline of lung function, Cthrc1 knockout (Cthrc1(-/-)) and wild-type mice (WT) received intratracheal injections of 2.5 U/kg bleomycin or saline...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28284148/effect-enhancing-and-toxicity-reducing-activity-of-usnic-acid-in-ascitic-tumor-bearing-mice-treated-with-bleomycin
#9
Zu-Qing Su, Yu-Hong Liu, Hui-Zhen Guo, Chao-Yue Sun, Jian-Hui Xie, Yu-Cui Li, Jian-Nan Chen, Xiao-Ping Lai, Zi-Ren Su, Hai-Ming Chen
Usnic acid (UA) can be found in certain lichen species. Growing evidence suggests that UA possesses antitumoral, antioxidative and anti-inflammatory activities. Bleomycin (BLM) is widely used in the treatment of malignant ascites, however, it unexpectedly causes pulmonary fibrosis (PF). Researches show that excessive inflammatory response and oxidative stress in lung tissue is conspicuous causes of BLM-induced PF. Here we investigated mechanism underlying the effect-enhancing and toxicity-reducing activity of UA on H22-bearing mice treated with BLM...
March 8, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28283856/effects-of-nintedanib-on-the-microvascular-architecture-in-a-lung-fibrosis-model
#10
Maximilian Ackermann, Yong Ook Kim, Willi L Wagner, Detlef Schuppan, Cristian D Valenzuela, Steven J Mentzer, Sebastian Kreuz, Detlef Stiller, Lutz Wollin, Moritz A Konerding
Nintedanib, a tyrosine kinase inhibitor approved for the treatment of idiopathic pulmonary fibrosis, has anti-fibrotic, anti-inflammatory, and anti-angiogenic activity. We explored the impact of nintedanib on microvascular architecture in a pulmonary fibrosis model. Lung fibrosis was induced in C57Bl/6 mice by intratracheal bleomycin (0.5 mg/kg). Nintedanib was started after the onset of lung pathology (50 mg/kg twice daily, orally). Micro-computed tomography was performed via volumetric assessment. Static lung compliance and forced vital capacity were determined by invasive measurements...
March 10, 2017: Angiogenesis
https://www.readbyqxmd.com/read/28283478/annexin-a2-contributes-to-lung-injury-and-fibrosis-by-augmenting-factor-xa-fibrogenic-activity
#11
Michael Schuliga, Jade Jaffar, Asres Berhan, Shenna Langenbach, Trudi Harris, David Waters, Peter Vee Sin Lee, Christopher Grainge, Glen Westall, Darryl Knight, Alastair G Stewart
In lung injury and disease, including idiopathic pulmonary fibrosis (IPF), extravascular factor X is converted into factor Xa (FXa), a coagulant protease with fibrogenic actions. Extracellular annexin A2 binds to FXa, augmenting activation of the protease activated receptor-1 (PAR-1). In this study, the contribution of annexin A2 in lung injury and fibrosis was investigated. Annexin A2 immunoreactivity was observed in regions of fibrosis, including associated with fibroblasts in lung tissue of IPF patients...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28283477/lung-epithelial-cell-focal-adhesion-kinase-signaling-inhibits-lung-injury-and-fibrosis
#12
Amanda K Wheaton, Manisha Agarwal, Shijing Jia, Kevin K Kim
Progressive pulmonary fibrosis is a devastating consequence of many acute and chronic insults to the lung. Lung injury leads to alveolar epithelial cell (AEC) death, destruction of the basement membrane and activation of TGFβ. There is subsequent resolution of the injury and a coordinated and concurrent initiation of fibrosis. Both of these processes may involve activation of similar intracellular signaling pathways regulated in part by dynamic changes to the extracellular matrix. Matrix signaling can augment the pro-fibrotic fibroblast response to TGFβ...
March 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28273952/comparative-analysis-of-lysyl-oxidase-like-family-members-in-pulmonary-fibrosis
#13
Verena Aumiller, Benjamin Strobel, Merrit Romeike, Michael Schuler, Birgit E Stierstorfer, Sebastian Kreuz
Extracellular matrix (ECM) composition and stiffness are major driving forces for the development and persistence of fibrotic diseases. Lysyl oxidase (LOX) and LOX-like (LOXL) proteins play crucial roles in ECM remodeling due to their collagen crosslinking and intracellular functions. Here, we systematically investigated LOX/L expression in primary fibroblasts and epithelial cells under fibrotic conditions, Bleomycin (BLM) induced lung fibrosis and in human IPF tissue. Basal expression of all LOX/L family members was detected in epithelial cells and at higher levels in fibroblasts...
December 2017: Scientific Reports
https://www.readbyqxmd.com/read/28273432/p53-and-mir-34a-feedback-promotes-lung-epithelial-injury-and-pulmonary-fibrosis
#14
Shwetha K Shetty, Nivedita Tiwari, Amarnath S Marudamuthu, Bijesh Puthusseri, Yashodhar P Bhandary, Jian Fu, Jeffrey Levin, Steven Idell, Sreerama Shetty
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease. The pathogenesis of interstitial lung diseases, including its most common form, IPF, remains poorly understood. Alveolar epithelial cell (AEC) apoptosis, proliferation, and accumulation of myofibroblasts and extracellular matrix deposition results in progressive loss of lung function in IPF. We found induction of tumor suppressor protein, p53, and apoptosis with suppression of urokinase-type plasminogen activator (uPA) and the uPA receptor in AECs from the lungs of IPF patients, and in mice with bleomycin, cigarette smoke, silica, or sepsis-induced lung injury...
March 5, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28263743/deficiency-of-psgl-1-accelerates-bleomycin-blm-induced-lung-fibrosis-and-inflammation-in-mice-through-activating-pi3k-akt
#15
Xiang Han, Shu-Ming Wang
Pulmonary fibrosis is a disease characterized by unremitting fibrosis accumulation in the lung, causing respiratory failure eventually. Presently, the immunological mechanism underlying pulmonary fibrosis still remains unclear. P-selectin glycoprotein ligand-1 (Psgl-1) is a leukocyte ligand that regulates recruitment and activation of multiple cell types, which is associated with phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway activation. In the present study, we attempted to clarify the AKT activation induced by Psgl-1 knockout in mice with bleomycin (BLM)-induced pulmonary fibrosis...
March 3, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28258190/sirt3-deficiency-promotes-lung-fibrosis-by-augmenting-alveolar-epithelial-cell-mitochondrial-dna-damage-and-apoptosis
#16
Renea P Jablonski, Seok-Jo Kim, Paul Cheresh, David B Williams, Luisa Morales-Nebreda, Yuan Cheng, Anjana Yeldandi, Sangeeta Bhorade, Annie Pardo, Moises Selman, Karen Ridge, David Gius, G R Scott Budinger, David W Kamp
Alveolar epithelial cell (AEC) mitochondrial dysfunction and apoptosis are important in idiopathic pulmonary fibrosis and asbestosis. Sirtuin 3 (SIRT3) detoxifies mitochondrial reactive oxygen species, in part, by deacetylating manganese superoxide dismutase (MnSOD) and mitochondrial 8-oxoguanine DNA glycosylase. We reasoned that SIRT3 deficiency occurs in fibrotic lungs and thereby augments AEC mtDNA damage and apoptosis. Human lungs were assessed by using immunohistochemistry for SIRT3 activity via acetylated MnSOD(K68) Murine AEC SIRT3 and cleaved caspase-9 (CC-9) expression were assayed by immunoblotting with or without SIRT3 enforced expression or silencing...
March 3, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28251930/amine-oxidase-activity-regulates-the-development-of-pulmonary-fibrosis
#17
Fumiko Marttila-Ichihara, Kati Elima, Kaisa Auvinen, Tibor Z Veres, Pia Rantakari, Christopher Weston, Masayuki Miyasaka, David Adams, Sirpa Jalkanen, Marko Salmi
In pulmonary fibrosis, an inflammatory reaction and differentiation of myofibroblasts culminate in pathologic deposition of collagen. Amine oxidase copper containing-3 (AOC3) is a cell-surface expressed oxidase that regulates leukocyte extravasation. Here we analyzed the potential role of AOC3 using gene-modified and inhibitor-treated mice in a bleomycin-induced pulmonary fibrosis model. Inflammation and fibrosis of lungs were assessed by histologic, flow cytometric, and quantitative PCR analysis. AOC3-deficient mice showed a 30-50% reduction in fibrosis, collagen synthesis, numbers of myofibroblasts, and accumulation of CD4(+) lymphocytes, NK T cells, macrophages, and type 2 innate lymphoid cells compared with wild-type control mice...
March 1, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28245556/supercritical-carbon-dioxide-fluid-extract-from-chrysanthemum-indicum-enhances-anti-tumor-effect-and-reduces-toxicity-of-bleomycin-in-tumor-bearing-mice
#18
Hong-Mei Yang, Chao-Yue Sun, Jia-Li Liang, Lie-Qiang Xu, Zhen-Biao Zhang, Dan-Dan Luo, Han-Bin Chen, Yong-Zhong Huang, Qi Wang, David Yue-Wei Lee, Jie Yuan, Yu-Cui Li
Bleomycin (BLM), a family of anti-tumor drugs, was reported to exhibit severe side effects limiting its usage in clinical treatment. Therefore, finding adjuvants that enhance the anti-tumor effect and reduce the detrimental effect of BLM is a prerequisite. Chrysanthemum indicum, an edible flower, possesses abundant bioactivities; the supercritical-carbon dioxide fluid extract from flowers and buds of C. indicum (CISCFE) have strong anti-inflammatory, anti-oxidant, and lung protective effects. However, the role of CISCFE combined with BLM treatment on tumor-bearing mice remains unclear...
February 24, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28230051/cellular-senescence-mediates-fibrotic-pulmonary-disease
#19
Marissa J Schafer, Thomas A White, Koji Iijima, Andrew J Haak, Giovanni Ligresti, Elizabeth J Atkinson, Ann L Oberg, Jodie Birch, Hanna Salmonowicz, Yi Zhu, Daniel L Mazula, Robert W Brooks, Heike Fuhrmann-Stroissnigg, Tamar Pirtskhalava, Y S Prakash, Tamara Tchkonia, Paul D Robbins, Marie Christine Aubry, João F Passos, James L Kirkland, Daniel J Tschumperlin, Hirohito Kita, Nathan K LeBrasseur
Idiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by interstitial remodelling, leading to compromised lung function. Cellular senescence markers are detectable within IPF lung tissue and senescent cell deletion rejuvenates pulmonary health in aged mice. Whether and how senescent cells regulate IPF or if their removal may be an efficacious intervention strategy is unknown. Here we demonstrate elevated abundance of senescence biomarkers in IPF lung, with p16 expression increasing with disease severity...
February 23, 2017: Nature Communications
https://www.readbyqxmd.com/read/28213468/microencapsulation-of-lefty-secreting-engineered-cells-for-pulmonary-fibrosis-therapy-in-mice
#20
Hongge Ma, Shupei Qiao, Zeli Wang, Shuai Geng, Yufang Zhao, Xiaolu Hou, Weiming Tian, Xiongbiao Chen, Lifen Yao
Idiopathic pulmonary fibrosis (IPF) is a progressive disease that causes unremitting deposition of extracellular matrix proteins, thus resulting in distortion of the pulmonary architecture and impaired gas exchange. Associated with high morbidity and mortality, IPF is generally refractory to current pharmacological therapies. Lefty A, a potent inhibitor of transforming growth factor (TGF)-β signaling, has been shown to have promising antifibrotic ability in vitro for the treatment of renal fibrosis and other potential organ fibroses...
February 17, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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