Inhibition of EP300 and DDR1 synergistically alleviates pulmonary fibrosis in vitro and in vivo
The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. [Display omitted] •Both EP300 and DDR1 were overexpressed in IPF tissues.•Overexpression of EP300 positive...
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Published in | Biomedicine & pharmacotherapy Vol. 106; pp. 1727 - 1733 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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France
Elsevier Masson SAS
01.10.2018
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Abstract | The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF.
[Display omitted]
•Both EP300 and DDR1 were overexpressed in IPF tissues.•Overexpression of EP300 positively regulated fibronectin and DDR1, but not affected DDR1 phosphorylation.•Novel DDR1 inhibitor CQ-061 and EP300 inhibitor (or siRNA) synergistically reversed the inflammatory and fibrotic pulmonary injure.•These can be considered as potential therapeutic approach against IPF for further development.
Pulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1) signaling plays an important role. EP300 is defined as an acetyltransferase that can acetylate histone and has been broadly studied in several chronic diseases, including cancer, inflammation and fibrosis. This study aimed to investigate the relationship between p300 and DDR1 in the pathological processes of pulmonary fibrosis.
Transcriptome analysis of single cell RNA-sequencing for idiopathic pulmonary fibrosis (IPF) bronchial epithelial cells demonstrated that both DDR1 and EP300 were up-regulated and involved in the regulation of autophagy, cellular response to organonitrogen compounds, and collagen metabolic pathways, respectively. The anti-fibrotic and anti-inflammation effects of Pim1 and DDR1 inhibitors in bleomycin-induced IPF murine models were estimated.
We discovered that overexpression of EP300 signaling induced MRC5 human fibroblast cells that up-regulated the expression of DDR1 and FN1; however, no effects on COL1 A1 and DDR1 phosphorylation were observed. Mechanistically, TGF-β1 activated FN1, collagen, and DDR1 signaling could be reversed by the combination of p300 siRNA and DDR1 inhibitors. Moreover, the EP300 inhibitor SGC-CBP30 displayed synergistic effects with DDR1 inhibitors in pathogenic scores, airway goblet cell counts in bronchoalveolar lavage fluid (BALF), IL-4, IFN-γ, FN1COL1 A1 secretion and α-SMA, a marker of myofibroblast.
The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in our pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. |
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AbstractList | OBJECTIVESPulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1) signaling plays an important role. EP300 is defined as an acetyltransferase that can acetylate histone and has been broadly studied in several chronic diseases, including cancer, inflammation and fibrosis. This study aimed to investigate the relationship between p300 and DDR1 in the pathological processes of pulmonary fibrosis.MATERIALS AND METHODSTranscriptome analysis of single cell RNA-sequencing for idiopathic pulmonary fibrosis (IPF) bronchial epithelial cells demonstrated that both DDR1 and EP300 were up-regulated and involved in the regulation of autophagy, cellular response to organonitrogen compounds, and collagen metabolic pathways, respectively. The anti-fibrotic and anti-inflammation effects of Pim1 and DDR1 inhibitors in bleomycin-induced IPF murine models were estimated.RESULTSWe discovered that overexpression of EP300 signaling induced MRC5 human fibroblast cells that up-regulated the expression of DDR1 and FN1; however, no effects on COL1 A1 and DDR1 phosphorylation were observed. Mechanistically, TGF-β1 activated FN1, collagen, and DDR1 signaling could be reversed by the combination of p300 siRNA and DDR1 inhibitors. Moreover, the EP300 inhibitor SGC-CBP30 displayed synergistic effects with DDR1 inhibitors in pathogenic scores, airway goblet cell counts in bronchoalveolar lavage fluid (BALF), IL-4, IFN-γ, FN1COL1 A1 secretion and α-SMA, a marker of myofibroblast.CONCLUSIONSThe EP300 siRNA and inhibitors sensitized DDR1 inhibitors in our pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. [Display omitted] •Both EP300 and DDR1 were overexpressed in IPF tissues.•Overexpression of EP300 positively regulated fibronectin and DDR1, but not affected DDR1 phosphorylation.•Novel DDR1 inhibitor CQ-061 and EP300 inhibitor (or siRNA) synergistically reversed the inflammatory and fibrotic pulmonary injure.•These can be considered as potential therapeutic approach against IPF for further development. Pulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1) signaling plays an important role. EP300 is defined as an acetyltransferase that can acetylate histone and has been broadly studied in several chronic diseases, including cancer, inflammation and fibrosis. This study aimed to investigate the relationship between p300 and DDR1 in the pathological processes of pulmonary fibrosis. Transcriptome analysis of single cell RNA-sequencing for idiopathic pulmonary fibrosis (IPF) bronchial epithelial cells demonstrated that both DDR1 and EP300 were up-regulated and involved in the regulation of autophagy, cellular response to organonitrogen compounds, and collagen metabolic pathways, respectively. The anti-fibrotic and anti-inflammation effects of Pim1 and DDR1 inhibitors in bleomycin-induced IPF murine models were estimated. We discovered that overexpression of EP300 signaling induced MRC5 human fibroblast cells that up-regulated the expression of DDR1 and FN1; however, no effects on COL1 A1 and DDR1 phosphorylation were observed. Mechanistically, TGF-β1 activated FN1, collagen, and DDR1 signaling could be reversed by the combination of p300 siRNA and DDR1 inhibitors. Moreover, the EP300 inhibitor SGC-CBP30 displayed synergistic effects with DDR1 inhibitors in pathogenic scores, airway goblet cell counts in bronchoalveolar lavage fluid (BALF), IL-4, IFN-γ, FN1COL1 A1 secretion and α-SMA, a marker of myofibroblast. The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in our pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. Pulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1) signaling plays an important role. EP300 is defined as an acetyltransferase that can acetylate histone and has been broadly studied in several chronic diseases, including cancer, inflammation and fibrosis. This study aimed to investigate the relationship between p300 and DDR1 in the pathological processes of pulmonary fibrosis. Transcriptome analysis of single cell RNA-sequencing for idiopathic pulmonary fibrosis (IPF) bronchial epithelial cells demonstrated that both DDR1 and EP300 were up-regulated and involved in the regulation of autophagy, cellular response to organonitrogen compounds, and collagen metabolic pathways, respectively. The anti-fibrotic and anti-inflammation effects of Pim1 and DDR1 inhibitors in bleomycin-induced IPF murine models were estimated. We discovered that overexpression of EP300 signaling induced MRC5 human fibroblast cells that up-regulated the expression of DDR1 and FN1; however, no effects on COL1 A1 and DDR1 phosphorylation were observed. Mechanistically, TGF-β1 activated FN1, collagen, and DDR1 signaling could be reversed by the combination of p300 siRNA and DDR1 inhibitors. Moreover, the EP300 inhibitor SGC-CBP30 displayed synergistic effects with DDR1 inhibitors in pathogenic scores, airway goblet cell counts in bronchoalveolar lavage fluid (BALF), IL-4, IFN-γ, FN1COL1 A1 secretion and α-SMA, a marker of myofibroblast. The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in our pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF. |
Author | Ou, Yu Tang, Xu Yu, Xiaoping Jiang, Qinglin Tao, Jia Wen, Zhijie Wang, Baoxue Zhang, Lei Zhang, Min |
Author_xml | – sequence: 1 givenname: Jia surname: Tao fullname: Tao, Jia organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China – sequence: 2 givenname: Min surname: Zhang fullname: Zhang, Min organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China – sequence: 3 givenname: Zhijie surname: Wen fullname: Wen, Zhijie organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China – sequence: 4 givenname: Baoxue surname: Wang fullname: Wang, Baoxue organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China – sequence: 5 givenname: Lei surname: Zhang fullname: Zhang, Lei organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China – sequence: 6 givenname: Yu surname: Ou fullname: Ou, Yu organization: Chengdu Medical College, Chengdu 610500, China – sequence: 7 givenname: Xu surname: Tang fullname: Tang, Xu email: tx200107083@sina.com organization: Chengdu Medical College Hospital, Chengdu Medical College, Chengdu 610500, China – sequence: 8 givenname: Xiaoping surname: Yu fullname: Yu, Xiaoping email: cyggwsyxp@sina.com organization: The Public Health Department, Chengdu Medical College, Chengdu 610500, China – sequence: 9 givenname: Qinglin orcidid: 0000-0002-4056-165X surname: Jiang fullname: Jiang, Qinglin email: jql_cmc@163.com organization: School of Pharmacy and Sichuan Province College Key Laboratory of Structure-Specific Small Molecule Drugs, Chengdu Medical College, Chengdu 610500, China |
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Keywords | EP300 Bleomycin Discoidin domain receptor Idiopathic pulmonary fibrosis |
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Snippet | The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with... Pulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1) signaling... OBJECTIVESPulmonary fibrosis is strongly correlated with inflammation factors, cytokine, and collagen secretion, whereby discoidin domain receptor 1 (DDR1)... |
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SubjectTerms | Animals Bleomycin Case-Control Studies Cell Line Discoidin domain receptor Discoidin Domain Receptor 1 - antagonists & inhibitors Discoidin Domain Receptor 1 - metabolism Disease Models, Animal Dose-Response Relationship, Drug Drug Synergism Drug Therapy, Combination E1A-Associated p300 Protein - antagonists & inhibitors E1A-Associated p300 Protein - genetics E1A-Associated p300 Protein - metabolism EP300 Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - pathology Fibronectins - metabolism Humans Idiopathic pulmonary fibrosis Lung - drug effects Lung - metabolism Lung - pathology Phosphorylation Pulmonary Fibrosis - drug therapy Pulmonary Fibrosis - genetics Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology Rats, Sprague-Dawley Respiratory System Agents - pharmacology RNA Interference RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Transforming Growth Factor beta1 - pharmacology |
Title | Inhibition of EP300 and DDR1 synergistically alleviates pulmonary fibrosis in vitro and in vivo |
URI | https://dx.doi.org/10.1016/j.biopha.2018.07.132 https://www.ncbi.nlm.nih.gov/pubmed/30119248 https://search.proquest.com/docview/2089856439 |
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