Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis (IPF) is a lethal disease with insufficient treatment strategies. Here the authors show that reduction of the microRNA MIRLET7D and hyperactivation of EP300 contribute to impaired epigenetic silencing by the MiCEE complex in pulmonary fibroblasts of IPF patients, and de...
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2019-05-01
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doaj-3d39e90c296449c8bbc1d8a1a253f05c2021-05-11T12:15:28ZengNature Publishing GroupNature Communications2041-17232019-05-0110111610.1038/s41467-019-10066-7Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosisKarla Rubio0Indrabahadur Singh1Stephanie Dobersch2Pouya Sarvari3Stefan Günther4Julio Cordero5Aditi Mehta6Lukasz Wujak7Hector Cabrera-Fuentes8Cho-Ming Chao9Peter Braubach10Saverio Bellusci11Werner Seeger12Andreas Günther13Klaus T. Preissner14Malgorzata Wygrecka15Rajkumar Savai16Dulce Papy-Garcia17Gergana Dobreva18Mathias Heikenwalder19Soni Savai-Pullamsetti20Thomas Braun21Guillermo Barreto22Lung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchLung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchLung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchDepartment of Lung Development and Remodeling, Max-Planck-Institute for Heart and Lung ResearchDepartment of Cardiac Development, Max-Planck-Institute for Heart and Lung ResearchLung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchLung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchFaculty of Medicine, Biochemistry Institute, Justus Liebig UniversityFaculty of Medicine, Biochemistry Institute, Justus Liebig UniversityChair for Lung Matrix Remodeling, Excellence Cluster Cardio Pulmonary System, Justus Liebig UniversityGerman Center of Lung Research (Deutsches Zentrum für Lungenforschung, DZL), UGMLCInstitute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal UniversityDepartment of Lung Development and Remodeling, Max-Planck-Institute for Heart and Lung ResearchMember of the Excellence Cluster Cardio Pulmonary System (ECCPS), The Universities of Giessen and Marburg Lung Center (UGMLC)Faculty of Medicine, Biochemistry Institute, Justus Liebig UniversityFaculty of Medicine, Biochemistry Institute, Justus Liebig UniversityDepartment of Lung Development and Remodeling, Max-Planck-Institute for Heart and Lung ResearchLaboratoire Croissance, Réparation et Régénération Tissulaires (CRRET), CNRS ERL 9215, Université Paris Est Créteil, Université Paris EstAnatomy and Developmental Biology, CBTM, Heidelberg UniversityDivision Chronic Inflammation and Cancer (F180), German Cancer Research Center (DKFZ)Department of Lung Development and Remodeling, Max-Planck-Institute for Heart and Lung ResearchDepartment of Cardiac Development, Max-Planck-Institute for Heart and Lung ResearchLung Cancer Epigenetic, Max-Planck-Institute for Heart and Lung ResearchIdiopathic pulmonary fibrosis (IPF) is a lethal disease with insufficient treatment strategies. Here the authors show that reduction of the microRNA MIRLET7D and hyperactivation of EP300 contribute to impaired epigenetic silencing by the MiCEE complex in pulmonary fibroblasts of IPF patients, and demonstrate the benefit of inhibiting EP300 for the treatment of IPF.https://doi.org/10.1038/s41467-019-10066-7 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Karla Rubio Indrabahadur Singh Stephanie Dobersch Pouya Sarvari Stefan Günther Julio Cordero Aditi Mehta Lukasz Wujak Hector Cabrera-Fuentes Cho-Ming Chao Peter Braubach Saverio Bellusci Werner Seeger Andreas Günther Klaus T. Preissner Malgorzata Wygrecka Rajkumar Savai Dulce Papy-Garcia Gergana Dobreva Mathias Heikenwalder Soni Savai-Pullamsetti Thomas Braun Guillermo Barreto |
spellingShingle |
Karla Rubio Indrabahadur Singh Stephanie Dobersch Pouya Sarvari Stefan Günther Julio Cordero Aditi Mehta Lukasz Wujak Hector Cabrera-Fuentes Cho-Ming Chao Peter Braubach Saverio Bellusci Werner Seeger Andreas Günther Klaus T. Preissner Malgorzata Wygrecka Rajkumar Savai Dulce Papy-Garcia Gergana Dobreva Mathias Heikenwalder Soni Savai-Pullamsetti Thomas Braun Guillermo Barreto Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis Nature Communications |
author_facet |
Karla Rubio Indrabahadur Singh Stephanie Dobersch Pouya Sarvari Stefan Günther Julio Cordero Aditi Mehta Lukasz Wujak Hector Cabrera-Fuentes Cho-Ming Chao Peter Braubach Saverio Bellusci Werner Seeger Andreas Günther Klaus T. Preissner Malgorzata Wygrecka Rajkumar Savai Dulce Papy-Garcia Gergana Dobreva Mathias Heikenwalder Soni Savai-Pullamsetti Thomas Braun Guillermo Barreto |
author_sort |
Karla Rubio |
title |
Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis |
title_short |
Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis |
title_full |
Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis |
title_fullStr |
Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis |
title_full_unstemmed |
Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis |
title_sort |
inactivation of nuclear histone deacetylases by ep300 disrupts the micee complex in idiopathic pulmonary fibrosis |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2019-05-01 |
description |
Idiopathic pulmonary fibrosis (IPF) is a lethal disease with insufficient treatment strategies. Here the authors show that reduction of the microRNA MIRLET7D and hyperactivation of EP300 contribute to impaired epigenetic silencing by the MiCEE complex in pulmonary fibroblasts of IPF patients, and demonstrate the benefit of inhibiting EP300 for the treatment of IPF. |
url |
https://doi.org/10.1038/s41467-019-10066-7 |
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