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Bleomycin pulmonary fibrosis

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https://www.readbyqxmd.com/read/27909724/hsp27-regulates-tgf-%C3%AE-mediated-lung-fibroblast-differentiation-through-the-smad3-and-erk-pathways
#1
Gang Wang, Hao Jiao, Jun-Nian Zheng, Xia Sun
Idiopathic pulmonary fibrosis (IPF) is a chronic lethal interstitial lung disease with unknown etiology. Recent studies have indicated that heat-shock protein 27 (HSP27) contributes to the pathogenesis of IPF through the regulation of epithelial-mesenchymal transition (EMT). However, the expression and role of HSP27 in fibroblasts during pulmonary fibrogenesis has not been investigated to date, at least to the best of our knowledge. In this study, we examined the expression of HSP27 in fibrotic lung tissue and fibroblasts from bleomycin (BLM)-challenged mice and human lung fibroblasts treated with transforming growth factor-β (TGF-β)...
November 28, 2016: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27895584/induced-pluripotent-stem-cells-inhibit-bleomycin-induced-pulmonary-fibrosis-in-mice-through-suppressing-tgf-%C3%AE-1-smad-mediated-epithelial-to-mesenchymal-transition
#2
Yan Zhou, Zhong He, Yuan Gao, Rui Zheng, Xiaoye Zhang, Li Zhao, Mingqi Tan
Pulmonary fibrosis is a progressive and irreversible fibrotic lung disorder with high mortality and few treatment options. Recently, induced pluripotent stem (iPS) cells have been considered as an ideal resource for stem cell-based therapy. Although, an earlier study demonstrated the therapeutic effect of iPS cells on pulmonary fibrosis, the exact mechanisms remain obscure. The present study investigated the effects of iPS cells on inflammatory responses, transforming growth factor (TGF)-β1 signaling pathway, and epithelial to mesenchymal transition (EMT) during bleomycin (BLM)-induced lung fibrosis...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27894300/pleural-inhibition-of-the-caspase-1-il-1%C3%AE-pathway-diminishes-profibrotic-lung-toxicity-of-bleomycin
#3
Olivier Burgy, Pierre-Simon Bellaye, Sebastien Causse, Guillaume Beltramo, Guillaume Wettstein, Pierre-Marie Boutanquoi, Françoise Goirand, Carmen Garrido, Philippe Bonniaud
BACKGROUND: Idiopathic and toxic pulmonary fibrosis are severe diseases starting classically in the subpleural area of the lung. It has recently been suggested that pleural mesothelial cells acquire a myofibroblast phenotype under fibrotic conditions induced by TGF-β1 or bleomycin. The importance and role of inflammation in fibrogenesis are still controversial. In this work, we explored the role of IL-1β/caspase-1 signaling in bleomycin lung toxicity and in pleural mesothelial cell transformation...
November 29, 2016: Respiratory Research
https://www.readbyqxmd.com/read/27878273/pi3k-akt-signaling-is-involved-in-the-pathogenesis-of-bleomycin%C3%A2-induced-pulmonary-fibrosis-via-regulation-of-epithelial%C3%A2-mesenchymal-transition
#4
Xiao-Ling Zhang, Rong-Ge Xing, Liang Chen, Chun-Rong Liu, Zhi-Gang Miao
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by chronic inflammation, fibroblast proliferation and extracellular matrix deposition. However, the molecular and cellular mechanisms underlying the pathogenesis of pulmonary fibrosis remain to be fully elucidated. The contribution of the phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt) pathway in fibrotic processes remains to be investigated. The aim of the present study was to investigate the role of the PI3K/Akt pathway in pulmonary fibrosis...
November 22, 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27871152/human-adipose-derived-mesenchymal-stem-cells-attenuate-early-stage-of-bleomycin-induced-pulmonary-fibrosis-comparison-with-pirfenidone
#5
Manoj Reddy, Lyle Fonseca, Shashank Gowda, Basavraj Chougule, Aarya Hari, Satish Totey
Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, invariably fatal fibrotic lung disease with no lasting option for therapy. Mesenchymal stem cells (MSCs) could be a promising modality for the treatment of IPF. Aim of the study was to investigate improvement in survivability and anti-fibrotic efficacy of human adipose-derived mesenchymal stem cells (AD-MSCs) in comparison with pirfenidone in the bleomycin-induced pulmonary fibrosis model. Methods: Human AD-MSCs were administered intravenously on day 3, 6 and 9 after an intra-tracheal challenge with bleomycin, whereas, pirfenidone was given orally in drinking water at the rate of 100 mg/kg body weight three times a day daily from day 3 onward...
November 30, 2016: International Journal of Stem Cells
https://www.readbyqxmd.com/read/27858165/nmr-study-of-the-effects-of-some-bleomycin-c-termini-on-the-structure-of-a-dna-hairpin-with-the-5-gc-3-binding-site
#6
Teresa E Lehmann, Sally A Murray, Azure D Ingersoll, Teresa M Reilly, Shelby E Follett, Kevin E Macartney, Mark H Harpster
The antibiotics known as bleomycins constitute a family of natural products clinically employed for the treatment of a wide spectrum of cancers. The drug acts as an antitumor agent by virtue of the ability of a metal complex of the antibiotic to cleave DNA. Bleomycins are differentiated by their C-terminal regions. Previous structural studies involving metal-bleomycin-DNA triads have allowed the identification of the bithiazole-(C-terminus substituent) segment in this molecule as the one that most closely interacts with DNA...
November 17, 2016: Journal of Biological Inorganic Chemistry: JBIC
https://www.readbyqxmd.com/read/27853171/de-ubiquitinating-enzyme-usp11-promotes-transforming-growth-factor-%C3%AE-1-signaling-through-stabilization-of-transforming-growth-factor-%C3%AE-receptor-ii
#7
A M Jacko, L Nan, S Li, J Tan, J Zhao, D J Kass, Y Zhao
The transforming growth factor β-1 (TGFβ-1) signaling pathway plays a central role in the pathogenesis of pulmonary fibrosis. Two TGFβ-1 receptors, TβRI and TβRII, mediate this pathway. TβRI protein stability, as mediated by the ubiquitin/de-ubiquitination system, has been well studied; however, the molecular regulation of TβRII still remains unclear. Here we reveal that a de-ubiquitinating enzyme, USP11, promotes TGFβ-1 signaling through de-ubiquitination and stabilization of TβRII. We elucidate the role that mitoxantrone (MTX), an USP11 inhibitor, has in the attenuation of TGFβ-1 signaling...
November 17, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27816453/glaucocalyxin-a-improves-survival-in-bleomycin-induced-pulmonary-fibrosis-in-mice
#8
Fei Yang, Yiren Cao, Jian Zhang, Tao You, Li Zhu
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with unclear etiology and poor prognosis. Despite numerous studies on the pathogenesis of IPF, only scant treatment options are available for the management of IPF. Glaucocalyxin A (GLA), an ent-Kaurane diterpenoid, has been demonstrated to exert anti-inflammatory, anti-neoplastic and anti-platelet activities. In this study, we evaluated the role of GLA as an anti-fibrotic agent in bleomycin-induced pulmonary fibrosis in mice and investigated the underlying mechanisms by which GLA attenuates lung fibrosis...
November 2, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27815257/sirt3-blocks-myofibroblast-differentiation-and-pulmonary-fibrosis-by-preventing-mitochondrial-dna-damage
#9
Samik Bindu, Vinodkumar B Pillai, Abhinav Kanwal, Sadhana Samant, Gokhan Mutlu, Eric Verdin, Nickolai O Dulin, Mahesh P Gupta
Myofibroblast differentiation is a key process in the pathogenesis of fibrotic diseases. Transforming growth factor-β1 (TGFβ1) is a powerful inducer of myofibroblast differentiation and is implicated in pathogenensis of tissue fibrosis. This study was undertaken to determine the role of mitochondrial deacetylase, SIRT3 in TGF-β1-induced myofibroblast differentiqtion in vitro and lung fibrosis in vivo. Treatment of human lung fibroblasts with TGFβ1 resulted in increased expression of fibrosis markers, smooth muscle alpha-actin (α-SMA), collagen-1 and fibronectin...
November 4, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/27811936/transglutaminase-2-is-dispensable-but-required-for-the-survival-of-mice-in-dextran-sulfate-sodium-induced-colitis
#10
Eui Man Jeong, Young Hoon Son, Yewon Choi, Jin-Hee Kim, Jin-Haeng Lee, Sung-Yup Cho, In-Gyu Kim
Transglutaminase 2 (TG2) is a ubiquitously expressed enzyme that catalyzes crosslinking, polyamination or deamidation of glutamine residues in proteins. It has been reported that TG2 is involved in the pathogenesis of various inflammatory diseases including celiac disease, pulmonary fibrosis, cystic fibrosis, multiple sclerosis and sepsis. Recently, using a mouse model of bleomycin-induced lung fibrosis, we showed that TG2 is required to trigger inflammation via the induction of T helper type 17 (Th17) cell differentiation in response to tissue damage...
November 4, 2016: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/27808577/topoisomerase-i-peptide-loaded-dendritic-cells-induce-autoantibody-response-as-well-as-skin-and-lung-fibrosis
#11
Heena Mehta, Philippe-Olivier Goulet, Vinh Nguyen, Gemma Pérez, Martial Koenig, Jean-Luc Senécal, Marika Sarfati
DNA Topoisomerase I (TopoI) is a candidate autoantigen for diffuse cutaneous systemic sclerosis (dcSSc) associated with fatal lung disease. Dendritic cells (DCs) contribute to bleomycin-induced lung fibrosis. However, the possibility that TopoI-loaded DCs are involved in the initiation and/or perpetuation of dcSSc has not been explored. Here, we show that immunization with TopoI peptide-loaded DCs induces anti-TopoI autoantibody response and long-term fibrosis. Mice were repeatedly immunized with unpulsed DCs or DCs loaded with either TOPOIA or TOPOIB peptides, selected from different regions of TopoI...
November 3, 2016: Autoimmunity
https://www.readbyqxmd.com/read/27805412/sod3-r213g-snp-blocks-murine-bleomycin-induced-fibrosis-and-promotes-resolution-of-inflammation
#12
Gary C Mouradian, Rohit Gaurav, Steve Pugliese, Karim El Kasmi, Brittany Hartman, Laura Hernandez-Lagunas, Kurt Stenmark, Russ P Bowler, Eva Nozik-Grayck
Loss of extracellular superoxide dismutase (SOD3) contributes to inflammatory and fibrotic lung diseases. The human SOD3 R213G polymorphism decreases matrix binding, redistributing SOD3 from the lung to extracellular fluids and protects against LPS induced alveolar inflammation. We utilized mice expressing a naturally occurring single nucleotide polymorphism (SNP), rs1799895, within the HBD of SOD3 which results in an amino acid substitution at position 213 (R213G mice) to test the hypothesis that the redistribution of SOD3 into the extracellular fluids would impart protection against bleomycin-induced lung fibrosis and secondary pulmonary hypertension (PH)...
November 2, 2016: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/27798371/oncostatin-m-preconditioned-mesenchymal-stem-cells-alleviate-bleomycin-induced-pulmonary-fibrosis-through-paracrine-effects-of-the-hepatocyte-growth-factor
#13
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...
October 18, 2016: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/27797602/bleomycin-increases-neutrophil-adhesion-to-human-vascular-endothelial-cells-independently-of-upregulation-of-icam-1-and-e-selectin
#14
James D Williamson, Laura R Sadofsky, Michael G Crooks, John Greenman, Simon P Hart
AIM OF THE STUDY: Bleomycin-induced lung disease is a serious complication of therapy characterized by alveolar injury, cytokine release, inflammatory cell recruitment, and eventually pulmonary fibrosis. The mechanisms underlying bleomycin-induced pulmonary fibrosis may be relevant to other progressive scarring diseases of the lungs. Pulmonary vascular endothelial cells are critically involved in immune cell extravasation at sites of injury through adhesion molecule expression and cytokine release...
October 31, 2016: Experimental Lung Research
https://www.readbyqxmd.com/read/27797599/pyrrolidinedithiocarbamate-attenuates-bleomycin-induced-pulmonary-fibrosis-in-rats-modulation-of-oxidative-stress-fibrosis-and-inflammatory-parameters
#15
Mai A Zaafan, Hala F Zaki, Amany I El-Brairy, Sanaa A Kenawy
OBJECTIVE: The current study aimed to investigate the modulatory effects of pyrrolidinedithiocarbamate (PDTC; 100 mg/kg) on bleomycin-induced pulmonary fibrosis (5 mg/kg; intratracheal) in rats. MATERIALS AND METHODS: Rats were randomly assigned to three groups: normal control, bleomycin control, and PDTC-treated groups. Lung injury was evaluated through histological examination, immunohistochemical detection of inducible nitric oxide synthase (iNOS) in lung tissue and evaluating the total and differential leucocytes count in bronchoalveolar lavage fluid...
October 31, 2016: Experimental Lung Research
https://www.readbyqxmd.com/read/27793816/the-transcription-factor-gli2-as-a-downstream-mediator-of-transforming-growth-factor-%C3%AE-induced-fibroblast-activation-in-ssc
#16
Ruifang Liang, Barbora Šumová, Cinzia Cordazzo, Tatjana Mallano, Yun Zhang, Thomas Wohlfahrt, Clara Dees, Andreas Ramming, Dorota Krasowska, Małgorzata Michalska-Jakubus, Oliver Distler, Georg Schett, Ladislav Šenolt, Jörg H W Distler
OBJECTIVES: Hedgehog signalling plays a critical role during the pathogenesis of fibrosis in systemic sclerosis (SSc). Besides canonical hedgehog signalling with smoothened (SMO)-dependent activation of GLI transcription factors, GLI can be activated independently of classical hedgehog ligands and receptors (so-called non-canonical pathways). Here, we aimed to evaluate the role of non-canonical hedgehog signalling in SSc and to test the efficacy of direct GLI inhibitors that target simultaneously canonical and non-canonical hedgehog pathways...
October 28, 2016: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/27790277/increased-cellular-nad-level-through-nqo1-enzymatic-action-has-protective-effects-on-bleomycin-induced-lung-fibrosis-in-mice
#17
Gi-Su Oh, Su-Bin Lee, Anjani Karna, Hyung-Jin Kim, AiHua Shen, Arpana Pandit, SeungHoon Lee, Sei-Hoon Yang, Hong-Seob So
BACKGROUND: Idiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet...
October 2016: Tuberculosis and Respiratory Diseases
https://www.readbyqxmd.com/read/27777976/epithelial-macrophage-interactions-determine-pulmonary-fibrosis-susceptibility-in-hermansky-pudlak-syndrome
#18
Lisa R Young, Peter M Gulleman, Chelsi W Short, Harikrishna Tanjore, Taylor Sherrill, Aidong Qi, Andrew P McBride, Rinat Zaynagetdinov, John T Benjamin, William E Lawson, Sergey V Novitskiy, Timothy S Blackwell
Alveolar epithelial cell (AEC) dysfunction underlies the pathogenesis of pulmonary fibrosis in Hermansky-Pudlak syndrome (HPS) and other genetic syndromes associated with interstitial lung disease; however, mechanisms linking AEC dysfunction and fibrotic remodeling are incompletely understood. Since increased macrophage recruitment precedes pulmonary fibrosis in HPS, we investigated whether crosstalk between AECs and macrophages determines fibrotic susceptibility. We found that AECs from HPS mice produce excessive MCP-1, which was associated with increased macrophages in the lungs of unchallenged HPS mice...
October 20, 2016: JCI Insight
https://www.readbyqxmd.com/read/27774992/emodin-ameliorates-bleomycin-induced-pulmonary-fibrosis-in-rats-by-suppressing-epithelial-mesenchymal-transition-and-fibroblast-activation
#19
Ruijuan Guan, Xia Wang, Xiaomei Zhao, Nana Song, Jimin Zhu, Jijiang Wang, Jin Wang, Chunmei Xia, Yonghua Chen, Danian Zhu, Linlin Shen
Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs)...
October 24, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27761647/the-pattern-of-elastic-fiber-breakdown-in-bleomycin-induced-pulmonary-fibrosis-may-reflect-microarchitectural-changes
#20
Xingjian Liu, Shuren Ma, Gerard Turino, Jerome Cantor
INTRODUCTION: Desmosine and isodesmosine (DID) are unique elastin crosslinks that may serve as biomarkers for elastic fiber degradation in chronic obstructive pulmonary disease. Previously, our laboratory found that the ratio of free to peptide-bound DID in bronchoalveolar lavage fluid (BALF) showed a significant positive correlation with the extent of airspace enlargement in an elastase model of pulmonary emphysema. To further evaluate this hypothesis, our laboratory measured this ratio in a bleomycin (BLM) model of pulmonary fibrosis, which involved different microarchitectural changes than those associated with pulmonary emphysema...
October 19, 2016: Lung
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