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EMT and pulmonary fibrosis

Masashi Kawami, Rika Harabayashi, Mioka Miyamoto, Risako Harada, Ryoko Yumoto, Mikihisa Takano
PURPOSE: Methotrexate (MTX) therapy of certain cancers and rheumatoid arthritis often induces serious interstitial lung complications including pulmonary fibrosis. In this study, we investigated the epithelial-mesenchymal transition (EMT) induced by MTX and by transforming growth factor (TGF)-β1 in the human alveolar epithelial cell line A549 in order to develop new strategies for the prevention of EMT. METHODS: First, we examined the effect of TGF-β1 and MTX on cell morphology and the expression of EMT-related mRNAs in A549 cells...
September 7, 2016: Lung
Yi-Chun Wang, Jing-Shi Liu, Hao-Ke Tang, Jing Nie, Ji-Xian Zhu, Ling-Ling Wen, Qu-Lian Guo
MicroRNA (miR)-221 plays an essential role in the epithelial-mesenchymal transition (EMT). High mobility group AT-hook 2 (HMGA2), is a key regulator of EMT. However, the role of miR‑221 in pulmonary fibrosis, and the association between miR‑221 and HMGA2 remain largely unknown. For this purpose, we examined the expression of miR‑221 and HMGA2 in human idiopathic pulmonary fibrosis (IPF) tissues and pulmonary cells, namely the adenocarcinoma A549 and human bronchial epithelium (HBE) cell lines, and found that the expression of miR‑221 was inhibited in both tissues and cells whereas high mRNA and protein expression of HMGA2 was observed...
October 2016: International Journal of Molecular Medicine
Yi Zhuang, Jinghong Dai, Yongsheng Wang, Huan Zhang, Xinxiu Li, Chunli Wang, Mengshu Cao, Yin Liu, Jingjing Ding, Hourong Cai, Deping Zhang, Yaping Wang
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease involving pulmonary injury associated with tissue repair, dysfunction and fibrosis. Recent studies indicate that some microRNAs (miRNAs) may play critical roles in the pathogenesis of pulmonary fibrosis. In this study, we aim to investigate whether miR-338* (miR-338-5p), which has been found to be associated with tumor progression, is associated with pathological process of pulmonary fibrosis. Balb/c mice were treated with bleomycin (BLM) to establish IPF models...
2016: American Journal of Translational Research
Osamu Watanabe, Takao Tsuji, Ryota Kikuchi, Masayuki Itoh, Hiroyuki Nakamura, Kazutetsu Aoshiba
Recent evidence suggests that epithelial-mesenchymal transition (EMT) is involved in the pathogenesis of airway obstructive diseases, such as chronic obstructive pulmonary disease, asthma and bronchiolitis obliterans syndrome after lung transplantation. However, whether EMT occurs in an experimental model of airway fibrosis is not well known. We explored evidence of EMT in a murine model of airway fibrosis induced by repeated exposure to naphthalene. Mice were administered intraperitoneal injections of naphthalene or corn oil vehicle once weekly for 14 consecutive weeks...
October 2016: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
Jia You, Jintao Wang, Linshen Xie, Chengwen Zhu, Jingyuan Xiong
Emerging evidences support that transforming growth factor β1 (TGF-β1) induced epithelial-mesenchymal transition (EMT) participates in the pathogenesis of pulmonary fibrosis and asthmatic airway remodeling. Recent studies demonstrated that apolipoprotein A-I (Apo A-I) is the only known substance that can resolve established pulmonary fibrotic nodules, and Apo A-I mimetic D-4F (a synthetic polypeptide consisting of 18 amino acids) plays an inhibitory role in murine asthmatic model. However, cellular mechanisms for such therapeutic effects of Apo A-I and D-4F remain to be elucidated...
October 2016: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
Kui-Jun Chen, Qing Li, Cang-Mei Wen, Zhao-Xia Duan, Jie Yuan Zhang, Chuan Xu, Jian-Min Wang
The epithelial-to-mesenchymal transition (EMT) is a crucial cellular event in wound healing, tissue repair, and cancer progression in adult tissues, with the interactions with numerous signals. In this study, we aimed to determine whether bleomycin (BLM), an agent that causes pulmonary fibrosis, induces the EMT of the alveolar epithelial cell line A549 and investigated the possible mechanisms. We examined the EMT involved changes in cell morphology, isoform switching of the fibroblast growth factor receptor 2 (FGFR2) by alternative splicing, and expression of the phenotypic markers including E-cadherin, vimentin, and α-SMA using RT-PCR, Western blotting, and immunofluorescence assays...
2016: Journal of Cancer
Yingxin Zhao, Bing Tian, Rovshan G Sadygov, Yueqing Zhang, Allan R Brasier
UNLABELLED: The airway epithelium is a semi-impermeable barrier whose disruption by growth factor reprogramming is associated with chronic airway diseases of humans. Transforming growth factor beta (TGFβ)-induced epithelial mesenchymal transition (EMT) plays important roles in airway remodeling characteristic of idiopathic lung fibrosis, asthma and chronic obstructive pulmonary disease (COPD). Inflammation of the airways leads to airway injury and tumor necrosis factor alpha (TNFα) plays an important pro-inflammatory role...
October 4, 2016: Journal of Proteomics
Xiang Huang, Weicheng Wang, Huaqin Yuan, Jing Sun, Lele Li, Xingxin Wu, Jinhua Luo, Yanhong Gu
Idiopathic pulmonary fibrosis (IPF) is a chronic and ultimately fatal disease, characterized by excessive accumulation of fibroblasts, extensive deposition of extracellular matrix, and destruction of alveolar architecture. IPF is associated with an epithelial-dependent fibroblast-activated process, termed the epithelial-to-mesenchymal transition (EMT). However, there is still a lack of strategies to target EMT for the treatment of IPF. Sunitinib, a small-molecule multi-targeted tyrosine kinase inhibitor, targets multiple kinases that may play an important role in developing pulmonary fibrosis...
2016: Tohoku Journal of Experimental Medicine
Ae Rin Baek, Ji Min Lee, Hyun Jung Seo, Jong Sook Park, June Hyuk Lee, Sung Woo Park, An Soo Jang, Do Jin Kim, Eun Suk Koh, Soo Taek Uh, Yong Hoon Kim, Choon Sik Park
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-β1-induced EMT in experimental lung fibrosis and clarify its mechanism of action...
July 2016: Tuberculosis and Respiratory Diseases
Ji Zhou, Wenjie You, Guangqiang Sun, Yixuan Li, Bi Chen, Jing Ai, Handong Jiang
Metastasis accounts for the majority of cancer-related deaths. Transforming growth factor β (TGF-β) is believed to promote late-stage cancer progression and metastasis by inducing epithelial-mesenchymal transition (EMT). We previously reported that MS80, a novel oligosaccharide sulfate, inhibits TGF-β1-induced pulmonary fibrosis by binding TGF-β1. In our study MS80 effectively inhibited TGF-β/Smad signaling in lung cancer cells, breast cancer cells, and model cell lines. In addition, MS80 inhibited TGF-β1-induced EMT, motility, and invasion in vitro...
October 2016: Journal of Pharmacology and Experimental Therapeutics
Lin Shi, Nian Dong, Xiaocong Fang, Xiangdong Wang
Pulmonary fibrosis is characterized by an extensive activation of fibrogenic cells and deposition of extracellular matrix (ECM). Transforming growth factor (TGF)-β1 plays a pivotal role in the pathogenesis of pulmonary fibrosis, probably through the epithelial- to-mesenchymal transition (EMT) and ECM production. The present study investigates potential mechanism by which TGF-β1 induces EMT and ECM production in the fibrogenesis of human lung epithelial cells during pulmonary fibrosis. The expression of EMT phenotype and other proteins relevant to fibrogenesis were measured and the cell bio-behaviours were assessed using Cell-IQ Alive Image Monitoring System...
July 15, 2016: Journal of Cellular and Molecular Medicine
X R Tian, X L Tian, H F Wang, Q Chang, R J Huo, D L Ying, G P Zheng
OBJECTIVE: To investigate the regulation effect of β-catenin pathway on transforming growth factor beta1 (TGF-β1) induced pulmonary pro-fibrosis. METHODS: The rat alveolar typeⅡ cells (RLE-6TN) were divided into four groups: A1.control group; B1.TGF-β1 group was treated with 5 μg/L TGF-β1; C1.pcDNA+ TGF-β1 group was transiently transfected with eukaryotic expression vector pcDNA3.0 (pcDNA) and followed by TGF-β1 treatment (5 μg/L); D1.F-(β-TrCP)-Ecad+ TGF-β1 group was transiently transfected with β-catenin protein knockout vector [F-(β-TrCP)-Ecad] and followed by TGF-β1 treatment (5 μg/L)...
June 28, 2016: Zhonghua Yi Xue za Zhi [Chinese medical journal]
Yu Mikami, Hirotaka Matsuzaki, Hideyuki Takeshima, Kosuke Makita, Yasuhiro Yamauchi, Takahide Nagase
Fibrosis is often involved in the pathogenesis of various chronic progressive diseases such as interstitial pulmonary disease. Pathological hallmark is the formation of fibroblastic foci, which is associated with the disease severity. Mesenchymal cells consisting of the fibroblastic foci are proposed to be derived from several cell sources, including originally resident intrapulmonary fibroblasts and circulating fibrocytes from bone marrow. Recently, mesenchymal cells that underwent epithelial-mesenchymal transition (EMT) have been also supposed to contribute to the pathogenesis of fibrosis...
2016: Journal of Visualized Experiments: JoVE
Jun-chao Yang, Lu Xu, Kang Song, Yuan Wang, Run-di Gao, Rui-lin Chen, Yu Cao
OBJECTIVE: To explore the effect of polydatin on the growth of TGF-β₁induced humanalveolar epithelium A549 cells and the mechanism of polydatin for inhibiting the process of epithelial-mesenchymal transition (EMT). METHODS: A549 cells in vitro cultured were randomly divided into five groups, i.e., the blank group, the control group, the low dose polydatin group, the middle dose polydatin group, the high dose polydatin group. Common culture fluid was added in A549 cells of the blank group...
April 2016: Chinese Journal of Integrated Traditional and Western Medicine
L Rong, J Wu, W Wang, R-P Zhao, X-W Xu, D Hu
OBJECTIVE: The aim of this study was to investigate the effect of resveratrol on the idiopathic bleomycin (BLM)-induced pulmonary fibrosis, which is increasingly recognized as an epithelial-to-mesenchymal transition (EMT)-associated disease. MATERIALS AND METHODS: We evaluated the effect of resveratrol on the BLM-induced fibrosis in a mouse model, via monitoring the pathological chance in mice lung, the mice body weight change and the mice death. And we also explored the regulation by BLM on (and) resveratrol on the expression and activity of Sirt 1 and on the expression of epithelial-to-mesenchymal transition (EMT)-associated markers in mice lung...
May 2016: European Review for Medical and Pharmacological Sciences
Bi Chen, Hou-Rong Cai, Shan Xue, Wen-Jie You, Bin Liu, Han-Dong Jiang
BACKGROUND AND OBJECTIVE: The roles of bile acid microaspiration and bile acid-activated farnesoid X receptor (FXR) in the pathogenesis of idiopathic pulmonary fibrosis (IPF) remain unclear. We hypothesized that bile acids activate alveolar epithelial cells (AECs) and lung fibroblasts, which may be regulated by FXR activation. METHODS: Human AECs and normal or IPF-derived lung fibroblast cells were incubated with the three major bile acids: lithocholic acid (LCA), deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA)...
August 2016: Respirology: Official Journal of the Asian Pacific Society of Respirology
Yu Ji, Yan-Nong Dou, Qian-Wen Zhao, Ji-Zhou Zhang, Yan Yang, Ting Wang, Yu-Feng Xia, Yue Dai, Zhi-Feng Wei
AIM: Paeoniflorin has shown to attenuate bleomycin-induced pulmonary fibrosis (PF) in mice. Because the epithelial-mesenchymal transition (EMT) in type 2 lung endothelial cells contributes to excessive fibroblasts and myofibroblasts during multiple fibrosis of tissues, we investigated the effects of paeoniflorin on TGF-β mediated pulmonary EMT in bleomycin-induced PF mice. METHODS: PF was induced in mice by intratracheal instillation of bleomycin (5 mg/kg). The mice were orally treated with paeoniflorin or prednisone for 21 d...
June 2016: Acta Pharmacologica Sinica
Ai Ge, Yuan Ma, Ya-Nan Liu, Ye-Shan Li, Hao Gu, Jia-Xiang Zhang, Qin-Xue Wang, Xiao-Ning Zeng, Mao Huang
AIMS: Epithelial-mesenchymal transition (EMT) plays a critical role in airway repair and remodeling in many respiratory diseases such as asthma and pulmonary fibrosis. The flavone aglycone, diosmetin, possesses anti-remodeling activity in a murine model of chronic asthma, but little is known about its effects on EMT. Herein, we investigated whether diosmetin inhibits transforming growth factor-β1 (TGF-β1)-induced EMT with underlying mechanisms in human bronchial epithelial (HBE) cells...
May 15, 2016: Life Sciences
Joong-Sun Kim, Yeonghoon Son, Myung-Gu Jung, Ye Ji Jeong, Sung-Ho Kim, Su-Jae Lee, Yoon-Jin Lee, Hae-June Lee
Radiation-induced lung injury (RILI) involves pneumonitis and fibrosis, and results in pulmonary dysfunction. Moreover, RILI can be a fatal complication of thoracic radiotherapy. The present study investigated the protective effect of geranylgeranlyacetone (GGA), an inducer of heat shock protein (HSP)70, on RILI using a C57BL/6 mouse model of RILI developing 6 months subsequent to exposure to 12.5 Gy thoracic radiation. GGA was administered 5 times orally prior and subsequent to radiation exposure, and the results were assessed by histological analysis and western blotting...
June 2016: Molecular Medicine Reports
Paola Tomei, Valentina Masola, Simona Granata, Gloria Bellin, Pierluigi Carratù, Miriam Ficial, Valentina Anna Ventura, Maurizio Onisto, Onofrio Resta, Giovanni Gambaro, Marco Chilosi, Antonio Lupo, Gianluigi Zaza
BACKGROUND: Everolimus (EVE) is a mammalian target of rapamycin inhibitor (mTOR-I) widely used in transplantation that may determine some severe adverse events, including pulmonary fibrosis. The pathogenic mechanism of mTOR-I-associated pulmonary toxicity is still unclear, but epithelial to mesenchymal transition (EMT) of bronchial/pulmonary cells may play a role. METHODS: Three cell lines-human type II pneumocyte-derived A549, normal bronchial epithelial, and bronchial epithelial homozygous for the delta F508 cystic fibrosis-causing mutation-were treated with EVE or tacrolimus at different concentrations...
March 29, 2016: Journal of Nephrology
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