Nature Communications (Nov 2018)
Myh10 deficiency leads to defective extracellular matrix remodeling and pulmonary disease
- Hyun-Taek Kim,
- Wenguang Yin,
- Young-June Jin,
- Paolo Panza,
- Felix Gunawan,
- Beate Grohmann,
- Carmen Buettner,
- Anna M. Sokol,
- Jens Preussner,
- Stefan Guenther,
- Sawa Kostin,
- Clemens Ruppert,
- Aditya M. Bhagwat,
- Xuefei Ma,
- Johannes Graumann,
- Mario Looso,
- Andreas Guenther,
- Robert S. Adelstein,
- Stefan Offermanns,
- Didier Y. R. Stainier
Affiliations
- Hyun-Taek Kim
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Wenguang Yin
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Young-June Jin
- Department of Pharmacology, Max Planck Institute for Heart and Lung Research
- Paolo Panza
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Felix Gunawan
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Beate Grohmann
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Carmen Buettner
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- Anna M. Sokol
- Scientific Service Group of Biomolecular Mass Spectrometry, Max Planck Institute for Heart and Lung Research
- Jens Preussner
- ECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research
- Stefan Guenther
- ECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research
- Sawa Kostin
- Scientific Service Group of Morphometry, Max Planck Institute for Heart and Lung Research
- Clemens Ruppert
- Biobank, University of Giessen & Marburg Lung Center (UGLMC)
- Aditya M. Bhagwat
- Bioinformatics Core, Weill Cornell Medicine - Qatar
- Xuefei Ma
- Laboratory of Molecular Cardiology, National Heart, Lung and Blood Institute, National Institutes of Health
- Johannes Graumann
- Scientific Service Group of Biomolecular Mass Spectrometry, Max Planck Institute for Heart and Lung Research
- Mario Looso
- ECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research
- Andreas Guenther
- Biobank, University of Giessen & Marburg Lung Center (UGLMC)
- Robert S. Adelstein
- Laboratory of Molecular Cardiology, National Heart, Lung and Blood Institute, National Institutes of Health
- Stefan Offermanns
- Department of Pharmacology, Max Planck Institute for Heart and Lung Research
- Didier Y. R. Stainier
- Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research
- DOI
- https://doi.org/10.1038/s41467-018-06833-7
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 13
Abstract
Abnormal alveolar development and homeostasis are common features of pulmonary disease. Here the authors show that Myh10 expression is reduced in emphysema patients, and that Myh10 loss of function impairs alveolar formation and lung morphogenesis via upregulation of matrix metalloproteinase activity and altered matrix remodeling.
