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EMT and pulmonary fibrosis

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https://www.readbyqxmd.com/read/28131417/mir-18a-5p-inhibits-sub-pleural-pulmonary-fibrosis-by-targeting-tgf-%C3%AE-receptor-ii
#1
Qian Zhang, Hong Ye, Fei Xiang, Lin-Jie Song, Li-Ling Zhou, Peng-Cheng Cai, Jian-Chu Zhang, Fan Yu, Huan-Zhong Shi, Yunchao Su, Jian-Bao Xin, Wan-Li Ma
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that typically leads to respiratory failure and death within 3-5 years of diagnosis. Sub-pleural pulmonary fibrosis is a pathological hallmark of IPF. Bleomycin treatment of mice is a an established pulmonary fibrosis model. We recently showed that bleomycin-induced epithelial-mesenchymal transition (EMT) contributes to pleural mesothelial cell (PMC) migration and sub-pleural pulmonary fibrosis. MicroRNA (miRNA) expression has recently been implicated in the pathogenesis of IPF...
January 25, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28115235/anti-fibrotic-effects-of-chronic-treatment-with-the-selective-fxr-agonist-obeticholic-acid-in-the-bleomycin-induced-rat-model-of-pulmonary-fibrosis
#2
Paolo Comeglio, Sandra Filippi, Erica Sarchielli, Annamaria Morelli, Ilaria Cellai, Francesca Corcetto, Chiara Corno, Elena Maneschi, Alessandro Pini, Luciano Adorini, Gabriella Barbara Vannelli, Mario Maggi, Linda Vignozzi
Farnesoid X receptor (FXR) activation by obeticholic acid (OCA) has been demonstrated to inhibit inflammation and fibrosis development in liver, kidney and intestine in multiple disease models. FXR activation has also been demonstrated to suppress the inflammatory response and to promote lung repair after lung injury. This study investigated the protective effects of OCA treatment (3 or 10mg/kg/day) on inflammation, tissue remodeling and fibrosis in the bleomycin-induced pulmonary fibrosis rat model. Effects of OCA treatment on morphological and molecular alterations of the lung, as well as remodeling of the alveoli and the right ventricle were also evaluated...
January 20, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/27989784/emodin-suppresses-tgf-%C3%AE-1-induced-epithelial-mesenchymal-transition-in-alveolar-epithelial-cells-through-notch-signaling-pathway
#3
Rundi Gao, Ruilin Chen, Yu Cao, Yuan Wang, Kang Song, Ya Zhang, Junchao Yang
Pulmonary fibrosis is characterized by the destruction of lung tissue architecture and the formation of fibrous foci, currently has no satisfactory treatment. Emodin is a component of Chinese herb that has been reported to be medicament on pancreatic fibrosis and liver fibrosis. However, its role in pulmonary fibrosis has not been established yet. In the present study, we investigated the hypothesis that Emodin plays an inhibitory role in TGF-β1 induced epithelial-mesenchymal transition (EMT) of alveolar epithelial cell, and Emodin exerts its effect through the Notch signaling pathway...
March 1, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/27982105/nrf2-inhibits-epithelial-mesenchymal-transition-by-suppressing-snail-expression-during-pulmonary-fibrosis
#4
Wencheng Zhou, Xiaoting Mo, Wenhui Cui, Zhihui Zhang, Delin Li, Liucheng Li, Liang Xu, Hongwei Yao, Jian Gao
Epithelial-mesenchymal transition (EMT) is a phenotype conversion that plays a critical role in the development of pulmonary fibrosis (PF). It is known that snail could regulate the progression of EMT. Nuclear factor erythroid 2 related factor 2 (Nrf2), a key regulator of antioxidant defense system, protects cells against oxidative stress. However, it is not known whether Nrf2 regulates snail thereby modulating the development of PF. Here, bleomycin (BLM) was intratracheally injected into both Nrf2-knockout (Nrf2(-/-)) and wild-type mice to compare the development of PF...
December 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27941755/fibroblastic-foci-covered-with-alveolar-epithelia-exhibiting-epithelial-mesenchymal-transition-destroy-alveolar-septa-by-disrupting-blood-flow-in-idiopathic-pulmonary-fibrosis
#5
Miki Yamaguchi, Sachie Hirai, Yusuke Tanaka, Toshiyuki Sumi, Masahiro Miyajima, Taijiro Mishina, Gen Yamada, Mitsuo Otsuka, Tadashi Hasegawa, Takashi Kojima, Toshiro Niki, Atsushi Watanabe, Hiroki Takahashi, Yuji Sakuma
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease of unknown cause. IPF has a distinct histopathological pattern of usual interstitial pneumonia in which fibroblastic foci (FF) represent the leading edge of fibrotic destruction of the lung. Currently there are three major hypotheses for how FF are generated: (1) from resident fibroblasts, (2) from bone marrow-derived progenitors of fibroblasts, and (3) from alveolar epithelial cells that have undergone epithelial-mesenchymal transition (EMT)...
December 12, 2016: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/27916556/micrornas-mediated-epithelial-mesenchymal-transition-in-fibrotic-diseases
#6
REVIEW
Xiao-Zhou Zou, Ting Liu, Zhi-Cheng Gong, Chang-Ping Hu, Zheng Zhang
MicroRNAs (miRNAs), a large family of small and highly conserved non-coding RNAs, regulate gene expression through translational repression or mRNA degradation. Aberrant expression of miRNAs underlies a spectrum of diseases including organ fibrosis. Recent evidence suggests that miRNAs contribute to organ fibrosis through mediating epithelial-mesenchymal transition (EMT). Alleviation of EMT has been proposed as a promising strategy against fibrotic diseases given the key role of EMT in fibrosis. miRNAs impact the expression of specific ligands, receptors, and signaling pathways, thus modulating EMT and consequently influencing fibrosis...
December 2, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27911568/nf%C3%AE%C2%BAb-mediates-mesenchymal-transition-remodeling-and-pulmonary-fibrosis-in-response-to-chronic-inflammation-by-viral-rna-patterns
#7
Bing Tian, Igor Patrikeev, Lorenzo Ochoa, Gracie Vargas, KarryAnne K Belanger, Julia Litvinov, Istvan Boldogh, Bill T Ameredes, Massoud Motamedi, Allan R Brasier
Airway remodeling is resultant of a complex multi-cellular response associated with a progressive decline of pulmonary function in patients with chronic airway disease. Here, repeated infections with respiratory viruses are linked with airway remodeling through largely unknown mechanisms. Although acute activation of the Toll like receptor (TLR)3 pathway by extracellular poly(I:C) induces innate signaling through the NFkB transcription factor in human small airway epithelial cells (hSAECs), prolonged (repetitive or tonic) poly(I:C) stimulation produces chronic stress fiber formation, mesenchymal transition and activation of a fibrotic program...
December 2, 2016: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/27909724/hsp27-regulates-tgf-%C3%AE-mediated-lung-fibroblast-differentiation-through-the-smad3-and-erk-pathways
#8
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)...
January 2017: 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
#9
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/27878256/melatonin-attenuates-tgf%C3%AE-1-induced-epithelial-mesenchymal-transition-in-lung-alveolar-epithelial-cells
#10
Na Yu, Yi-Tian Sun, Xin-Ming Su, Miao He, Bing Dai, Jian Kang
Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease. However, the pathogenesis remains to be fully elucidated. Melatonin is secreted by the pineal gland, it has a strong antioxidant effect, and exerts an anti-fibrosis effect. Whether melatonin attenuates pulm -onary fibrosis by inhibiting epithelial‑mesenchymal transition (EMT) requires further research. The present study aimed to investigate whether melatonin prevents transforming growth factor‑β1 (TGF‑β1)‑induced EMT and underlying signaling pathways using reverse transcription‑quantitative polymerase chain reaction, western blot analysis and immunofluorescence...
December 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27793799/brd4-mediates-nf-%C3%AE%C2%BAb-dependent-epithelial-mesenchymal-transition-and-pulmonary-fibrosis-via-transcriptional-elongation
#11
Bing Tian, Yingxin Zhao, Hong Sun, Yueqing Zhang, Jun Yang, Allan R Brasier
Chronic epithelial injury triggers a TGF-β-mediated cellular transition from normal epithelium into a mesenchymal-like state that produces subepithelial fibrosis and airway remodeling. Here we examined how TGF-β induces the mesenchymal cell state and determined its mechanism. We observed that TGF-β stimulation activates an inflammatory gene program controlled by the NF-κB/RelA signaling pathway. In the mesenchymal state, NF-κB-dependent immediate-early genes accumulate euchromatin marks and processive RNA polymerase...
December 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/27790277/increased-cellular-nad-level-through-nqo1-enzymatic-action-has-protective-effects-on-bleomycin-induced-lung-fibrosis-in-mice
#12
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/27774992/emodin-ameliorates-bleomycin-induced-pulmonary-fibrosis-in-rats-by-suppressing-epithelial-mesenchymal-transition-and-fibroblast-activation
#13
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/27604426/methotrexate-induced-epithelial-mesenchymal-transition-in-the-alveolar-epithelial-cell-line-a549
#14
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
https://www.readbyqxmd.com/read/27513632/mir%C3%A2-221-targets-hmga2-to-inhibit-bleomycin%C3%A2-induced-pulmonary-fibrosis-by-regulating-tgf%C3%A2-%C3%AE-1-smad3-induced-emt
#15
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
https://www.readbyqxmd.com/read/27508042/mir-338-targeting-smoothened-to-inhibit-pulmonary-fibrosis-by-epithelial-mesenchymal-transition
#16
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
https://www.readbyqxmd.com/read/27498952/little-evidence-for-epithelial-mesenchymal-transition-in-a-murine-model-of-airway-fibrosis-induced-by-repeated-naphthalene-exposure
#17
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
https://www.readbyqxmd.com/read/27495007/d-4f-an-apolipoprotein-a-i-mimetic-inhibits-tgf-%C3%AE-1-induced-epithelial-mesenchymal-transition-in-human-alveolar-epithelial-cell
#18
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
https://www.readbyqxmd.com/read/27471572/bleomycin-blm-induces-epithelial-to-mesenchymal-transition-in-cultured-a549-cells-via-the-tgf-%C3%AE-smad-signaling-pathway
#19
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
https://www.readbyqxmd.com/read/27461979/integrative-proteomic-analysis-reveals-reprograming-tumor-necrosis-factor-signaling-in-epithelial-mesenchymal-transition
#20
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
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