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EMT and pulmonary fibrosis

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https://www.readbyqxmd.com/read/28725012/phycocyanin-attenuates-pulmonary-fibrosis-via-the-tlr2-myd88-nf-%C3%AE%C2%BAb-signaling-pathway
#1
Chengcheng Li, Yan Yu, Wenjun Li, Bo Liu, Xudong Jiao, Xinyu Song, Changjun Lv, Song Qin
Our aim was to investigate the effects of phycocyanin (PC) on bleomycin (BLM)-induced pulmonary fibrosis (PF). In this study, C57 BL/6 wild-type (WT) mice and toll-like receptor (TLR) 2 deficient mice were treated with PC for 28 days following BLM exposure. Serum and lung tissues were collected on days 3, 7 and 28. Data shows PC significantly decreased the levels of hydroxyproline (HYP), vimentin, surfactant-associated protein C (SP-C), fibroblast specific protein-1 (S100A4) and α-smooth muscle actin (α-SMA) but dramatically increased E-cadherin and podoplanin (PDPN) expression on day 28...
July 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28720386/cdc42-interacting-protein-4-silencing-relieves-pulmonary-fibrosis-in-stz-induced-diabetic-mice-via-the-wnt-gsk-3%C3%AE-%C3%AE-catenin-pathway
#2
Xiaoping Zhang, Ying Liu, Runxia Shao, Wei Li
Cdc42-interacting protein-4 (CIP4) has been reported to be closely associated with diabetic nephropathy in rat. However, little is known about the correlation between CIP4 and diabetic pulmonary fibrosis (PF) in mice. Here, diabetes was induced by streptozotocin (STZ), and later lung tissue was collected and subjected to hematoxylin and eosin (H & E) staining for morphological examination. The distinct up-regulation of CIP4 was observed in diabetic PF mice. CIP4 silencing increased overall weight and decreased lung weight...
July 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28714804/cellular-proliferation-and-differentiation-induced-by-single-layer-molybdenum-disulfide-and-mediation-mechanisms-of-proteins-via-the-akt-mtor-p70s6k-signaling-pathway
#3
Wei Zou, Xingli Zhang, Mengyang Zhao, Qixing Zhou, Xiangang Hu
Single-layer molybdenum disulfide (SLMoS2) is a novel kind of 2D nanosheet that has attracted great attention regarding its use in biosensors, drug delivery, tissue engineering and therapy. However, our results demonstrated that SLMoS2 accelerated proliferation and promoted myogenic differentiation and epithelial-mesenchymal transition (EMT) in human embryonic lung fibroblasts (HELFs). The abnormal proliferation and differentiation of HELFs contribute to idiopathic pulmonary fibrosis. Specifically, SLMoS2 significantly stimulated the expression of myofibroblast- and mesenchymal-associated genes and proteins...
July 17, 2017: Nanotoxicology
https://www.readbyqxmd.com/read/28699703/a-positive-feedback-loop-promotes-hif-1%C3%AE-stability-through-mir-210-mediated-suppression-of-runx3-in-paraquat-induced-emt
#4
Yong Zhu, Jinfeng Wang, Xiaoxiao Meng, Hui Xie, Jiuting Tan, Xinkun Guo, Peng Han, Ruilan Wang
Irreversible pulmonary fibrosis induced by paraquat (PQ) poisoning is the major cause of death in patients with PQ poisoning. The epithelial-mesenchymal transition (EMT) is postulated to be one of the main mechanisms of pulmonary fibrosis. Here, we investigated the role of miR-210 in PQ-induced EMT and its relationship with hypoxia-inducible factor-1α (HIF-1α). Western blotting, immunofluorescence, immunoprecipitation and other methods were used in this study. We found that miR-210 expression was significantly increased after PQ poisoning, and it may be regulated by HIF-1α...
July 12, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28694203/soluble-epoxide-hydrolase-inhibitor-auda-decreases-bleomycin-induced-pulmonary-toxicity-in-mice-by-inhibiting-the-p38-smad3-pathways
#5
Xin-Wei Dong, Yong-Liang Jia, Ling-Tian Ge, Bo Jiang, Jun-Xia Jiang, Jian Shen, Ya-Chao Jin, Yan Guan, Yun Sun, Qiang-Min Xie
Bleomycin (BLM) has potent tumor cell-killing properties that have given it an important place in cancer chemotherapy, but pulmonary toxicity is its major adverse effect. Soluble epoxide hydrolase (sEH) inhibitors have been reported to have protective effects in fibrosis models, but the effects of AUDA, an sEH inhibitor of BLM-induced pulmonary toxicity and fibrosis, remain to be researched. In this study, we assessed the effects of AUDA on the BLM-induced pulmonary fibrosis in a mouse model, and transforming growth factor (TGF)-β1-induced epithelial proliferation and epithelial-mesenchymal transition (EMT) in vitro by monitoring changes in pulmonary function, inflammatory response, fibrotic remodeling, and signaling pathways...
July 8, 2017: Toxicology
https://www.readbyqxmd.com/read/28693256/pirfenidone-may-revert-the-epithelial-to-mesenchymal-transition-in-human-lung-adenocarcinoma
#6
Ryota Kurimoto, Takahiro Ebata, Shunichiro Iwasawa, Tsukasa Ishiwata, Yuji Tada, Koichiro Tatsumi, Yuichi Takiguchi
The epithelial-to-mesenchymal transition (EMT) in cancer is associated with invasion, metastasis and chemoresistance. Recent studies have revealed the increased expression of programmed death-ligand 1 (PD-L1) in cells undergoing EMT. The underlying mechanism of EMT involves transforming growth factor-β (TGF-β) and fibroblast growth factor-2 (FGF-2). Pirfenidone and the known EMT-suppressor nintedanib suppress pulmonary fibrosis partially through suppression of TGF-β. The present study aimed to determine whether pirfenidone has the potential to induce EMT-reversion, using nintedanib as a reference...
July 2017: Oncology Letters
https://www.readbyqxmd.com/read/28678431/epithelial-to-mesenchymal-transition-and-its-role-in-egfr-mutant-lung-adenocarcinoma-and-idiopathic-pulmonary-fibrosis
#7
REVIEW
Yuji Sakuma
Lung adenocarcinoma cells with activating epidermal growth factor receptor (EGFR) mutations are highly dependent upon EGFR signaling for survival and undergo apoptosis when EGFR signaling is inhibited by tyrosine kinase inhibitor (TKI) treatment. Paradoxically, EGFR-mutant lung adenocarcinomas have subpopulations of cells that can survive independently of activated EGFR. Such EGFR-independent EGFR-mutant cancer cells include cells that have undergone epithelial-to-mesenchymal transition (EMT) or transformed to small cell lung cancer, which almost completely lack EGFR dependency...
July 5, 2017: Pathology International
https://www.readbyqxmd.com/read/28667660/signaling-pathways-and-their-mirna-regulators-involved-in-the-etiopathology-of-idiopathic-pulmonary-fibrosis-ipf-and-hypersensitivity-pneumonitis-hp
#8
Justyna Kiszałkiewicz, Wojciech Piotrowski, Ewa Brzeziańska-Lasota
Idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP) belong to heterogenic group of interstitial lung diseases (ILD). For the reason that this group of diseases present with complex clinical non-specific features, they represent a diagnostic and therapeutic challenge. In this review we focus on several crucial signaling pathways participating in inflammation, fibrosis and EMT processes, so important in the course of ILD: TNF-α/NFκβ, TGF-β/SMAD, Wnt-β-catenin and PI3K-Akt signaling...
2017: Advances in Respiratory Medicine
https://www.readbyqxmd.com/read/28646553/epithelial-mesenchymal-transition-emt-a-spectrum-of-states-role-in-lung-development-homeostasis-and-disease
#9
REVIEW
Mohit Kumar Jolly, Chris Ward, Mathew Suji Eapen, Stephen Myers, Oskar Hallgren, Herbert Levine, Sukhwinder Singh Sohal
Epithelial Mesenchymal Transition (EMT) plays key roles during lung development and many lung diseases such as Chronic Obstructive Pulmonary Disease (COPD), lung cancer and pulmonary fibrosis. Here, integrating morphological observations with underlying molecular mechanisms, we highlight the functional role of EMT in lung development and injury repair, and discuss how it can contribute to pathogenesis of chronic lung disease. We discuss the evidence of manifestation of EMT and its potential driving role in COPD, idiopathic pulmonary fibrosis (IPF), bronchiolitis obliterans syndrome (BOS), and lung cancer, while noting that all cells need not display a full EMT in any of these contexts, i...
June 24, 2017: Developmental Dynamics: An Official Publication of the American Association of Anatomists
https://www.readbyqxmd.com/read/28624451/rapamycin-protects-against-paraquat-induced-pulmonary-fibrosis-activation-of-nrf2-signaling-pathway
#10
Yiheng Xu, Wenlin Tai, Xiaoyuan Qu, Wenjuan Wu, ZhenKun Li, Shuhao Deng, Chanthasone Vongphouttha, Zhaoxing Dong
Paraquat (PQ) is a widely used herbicide indeveloping countries worldwide, and pulmonary fibrosis is one of the most typical features of PQ poisoning. The molecular mechanism of PQ toxicity especially how to treat PQ-induced pulmonary fibrosis is still largely unknown. In animal model of pulmonary fibrosis, we used HE staining, western blotting assay and Real-time PCR assay to analyze the effects of rapamycin on the PQ-induced epithelial mesenchymal transition (EMT). We found that PQ induced the pulmonary fibrosis using HE staining and Masson's staining, and up-regulated the activity of HYP and the mRNA expressions of Collagen I and III (COL-1and COL-3) in pulmonary tissues...
August 19, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28598023/nintedanib-reduces-ventilation-augmented-bleomycin-induced-epithelial-mesenchymal-transition-and-lung-fibrosis-through-suppression-of-the-src-pathway
#11
Li-Fu Li, Kuo-Chin Kao, Yung-Yang Liu, Chang-Wei Lin, Ning-Hung Chen, Chung-Shu Lee, Chih-Wei Wang, Cheng-Ta Yang
Mechanical ventilation (MV) used in patients with acute respiratory distress syndrome (ARDS) can increase lung inflammation and pulmonary fibrogenesis. Src is crucial in mediating the transforming growth factor (TGF)-β1-induced epithelial-mesenchymal transition (EMT) during the fibroproliferative phase of ARDS. Nintedanib, a multitargeted tyrosine kinase inhibitor that directly blocks Src, has been approved for the treatment of idiopathic pulmonary fibrosis. The mechanisms regulating interactions among MV, EMT and Src remain unclear...
June 9, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28591554/nlrp3-participates-in-the-regulation-of-emt-in-bleomycin-induced-pulmonary-fibrosis
#12
Rui Tian, Yong Zhu, Jiayi Yao, Xiaoxiao Meng, Jinfeng Wang, Hui Xie, Ruilan Wang
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and irreversible lung disease. Studies have shown that epithelial-mesenchymal transition (EMT) plays an important role in the development of IPF. The NLRP3 inflammasome is reported to be activated and play an important role in many respiratory diseases. However, whether the NLRP3 inflammasome is activated in alveolar epithelial cells as well as the regulatory role of NLRP3 in EMT have not been reported. In this study, we transfected NLRP3 siRNA into A549 and RLE-6TN cells and treated them with bleomycin (BLM) for 24h...
June 4, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28588349/distinct-roles-of-wnt-%C3%AE-catenin-signaling-in-the-pathogenesis-of-chronic-obstructive-pulmonary-disease-and-idiopathic-pulmonary-fibrosis
#13
REVIEW
Juan Shi, Feng Li, Meihui Luo, Jun Wei, Xiaoming Liu
Wnt signaling pathways are tightly controlled under a physiological condition, under which they play key roles in many biological functions, including cell fate specification and tissue regeneration. Increasing lines of evidence recently demonstrated that a dysregulated activation of Wnt signaling, particularly the Wnt/β-catenin signaling, was involved in the pathogenesis of chronic pulmonary diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). In this respect, Wnt signaling interacts with other cellular signaling pathways to regulate the initiation and pathogenic procedures of airway inflammation and remodeling, pulmonary myofibroblast proliferation, epithelial-to-mesenchymal transition (EMT), and development of emphysema...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28540808/exposure-to-febrile-range-hyperthermia-potentiates-wnt-signalling-and-epithelial-mesenchymal-transition-gene-expression-in-lung-epithelium
#14
Ratnakar Potla, Mohan E Tulapurkar, Irina G Luzina, Sergei P Atamas, Ishwar S Singh, Jeffrey D Hasday
BACKGROUND: As environmental and body temperatures vary, lung epithelial cells experience temperatures significantly different from normal core temperature. Our previous studies in human lung epithelium showed that: (i) heat shock accelerates wound healing and activates profibrotic gene expression through heat shock factor-1 (HSF1); (ii) HSF1 is activated at febrile temperatures (38-41 °C) and (iii) hypothermia (32 °C) activates and hyperthermia (39.5 °C) reduces expression of a subset of miRNAs that target protein kinase-Cα (PKCα) and enhance proliferation...
April 26, 2017: International Journal of Hyperthermia
https://www.readbyqxmd.com/read/28522797/protective-effects-of-hydrogen-rich-saline-against-lipopolysaccharide-induced-alveolar-epithelial-to-mesenchymal-transition-and-pulmonary-fibrosis
#15
Wen-Wen Dong, Yun-Qian Zhang, Xiao-Yan Zhu, Yan-Fei Mao, Xue-Jun Sun, Yu-Jian Liu, Lai Jiang
BACKGROUND Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis. MATERIAL AND METHODS Male ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels...
May 19, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28493530/m2-macrophages-induce-emt-through-the-tgf-%C3%AE-smad2-signaling-pathway
#16
Liangying Zhu, Xiao Fu, Xiang Chen, Xiaodong Han, Ping Dong
IPF is characterized by fibroblast accumulation, collagen deposition and ECM remodeling, with myofibroblasts believed to be the effector cell type. Myofibroblasts develop due to EMT of lung alveolar epithelial cells, which can be induced by TGF-β. M2 macrophages, a macrophage subpopulation, secrete large amounts of TGF-β. To clarify the relationship between IPF, EMT, TGF-β and M2 macrophages, a bleomycin-induced pulmonary fibrosis mouse model was used. Seventeen days after mice were treated with bleomycin, the successful establishment of a pulmonary fibrosis model was confirmed by HE stain and Masson's trichrome stain...
May 11, 2017: Cell Biology International
https://www.readbyqxmd.com/read/28466866/posttreatment-with-protectin-dx-ameliorates-bleomycin-induced-pulmonary-fibrosis-and-lung-dysfunction-in-mice
#17
Hui Li, Yu Hao, Huawei Zhang, Weiyang Ying, Dan Li, Yahe Ge, Binyu Ying, Bihuan Cheng, Qingquan Lian, Shengwei Jin
Protectin DX (10S,17S-dihydroxydocosa-4Z,7Z,11E,13Z,15E,19Z-hexaenoic acid) (PDX), generated from Ω-3 fatty docosahexaenoic acids, is believed to exert anti-inflammatory and proresolution bioactions. To date, few studies have been performed regarding its effect on pulmonary fibrosis. Herein we show that PDX exerts a potential therapeutic effect which is distinct from its anti-inflammation and pro-resolution activity on mice with pulmonary fibrosis. In the present study, we showed that bleomycin (BLM) increased inflammatory infiltration, collagen deposition, and lung dysfunction on day7 after challenged in mice...
May 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28424456/paraquat-poisoning-induced-pulmonary-epithelial-mesenchymal-transition-through-notch1-pathway
#18
Tiegang Li, Xiangming Yang, Shiyu Xin, Yan Cao, Nana Wang
Progressive pulmonary fibrosis is the most characteristic feature of subacute PQ poisoning. Epithelial-to-mesenchymal transition (EMT) is reported to be involved in the pulmonary fibrosis after PQ exposure. Recent evidence suggested Notch signaling is required for EMT. In this study, we investigated whether Notch1 and TGF-β1/Smad3 signaling was involved in EMT caused by PQ. It is demonstrated that A549 cells underwent EMT after treated with PQ at dose of 300 μmol/L for 6 days, charactered by increasing expression of mesenchymal marker α-SMA and decreasing expression of epithelial marker E-cadherin...
April 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28408209/role-of-mir-34a-in-tgf-%C3%AE-1-and-drug-induced-epithelial-mesenchymal-transition-in-alveolar-type-ii-epithelial-cells
#19
Mikihisa Takano, Chinami Nekomoto, Masashi Kawami, Ryoko Yumoto
Epithelial-mesenchymal transition (EMT) of alveolar type II epithelial cells may play an important role in the pulmonary fibrosis induced by drugs such as bleomycin (BLM) and methotrexate (MTX). In this study, we examined the role of microRNAs (miRNAs) in drug-induced EMT using RLE/Abca3, a cell line having alveolar type II cell-like phenotype. Based on the screening using miRNA microarray analysis, it was found that the expression of some miRNAs, such as miR-34a, was increased by transforming growth factor (TGF)-β1 and BLM...
April 10, 2017: Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28386365/calpain-1-regulates-tgf-%C3%AE-1-induced-epithelial-mesenchymal-transition-in-human-lung-epithelial-cells-via-pi3k-akt-signaling-pathway
#20
Wei-Jun Tan, Qiu-Yue Tan, Ting Wang, Min Lian, Li Zhang, Zhen-Shun Cheng
Cell proliferation, transformation, and epithelial-mesenchymal transition (EMT) are key processes involved in the development of idiopathic pulmonary fibrosis (IPF). This study investigated the regulatory factors and signaling pathways that mediate EMT in the human type II alveolar epithelial A549 cell line. A549 cells were cultured in RPMI-1640 medium and allocated to the following four groups: blank control group or treated with transforming growth factor-β1 (TGF-β1), TGF-β1 + PD 150606 (a calpain 1 inhibitor), or PD 150606...
2017: American Journal of Translational Research
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