Communications Biology (Nov 2022)
An organ-on-chip model of pulmonary arterial hypertension identifies a BMPR2-SOX17-prostacyclin signalling axis
- Alexander J. Ainscough,
- Timothy J. Smith,
- Maike Haensel,
- Christopher J. Rhodes,
- Adam Fellows,
- Harry J. Whitwell,
- Eleni Vasilaki,
- Kelly Gray,
- Adrian Freeman,
- Luke S. Howard,
- John Wharton,
- Benjamin Dunmore,
- Paul D. Upton,
- Martin R. Wilkins,
- Joshua B. Edel,
- Beata Wojciak-Stothard
Affiliations
- Alexander J. Ainscough
- National Heart and Lung Institute, Imperial College London
- Timothy J. Smith
- Department of Chemistry, Imperial College London
- Maike Haensel
- National Heart and Lung Institute, Imperial College London
- Christopher J. Rhodes
- National Heart and Lung Institute, Imperial College London
- Adam Fellows
- National Heart and Lung Institute, Imperial College London
- Harry J. Whitwell
- National Phenome Centre and Imperial Clinical Phenotyping Centre, Department of Metabolism, Digestion and Reproduction, Imperial College London
- Eleni Vasilaki
- National Heart and Lung Institute, Imperial College London
- Kelly Gray
- Emerging Innovations Unit, Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca
- Adrian Freeman
- Emerging Innovations Unit, Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca
- Luke S. Howard
- National Heart and Lung Institute, Imperial College London
- John Wharton
- National Heart and Lung Institute, Imperial College London
- Benjamin Dunmore
- Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke’s and Royal Papworth Hospitals
- Paul D. Upton
- Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke’s and Royal Papworth Hospitals
- Martin R. Wilkins
- National Heart and Lung Institute, Imperial College London
- Joshua B. Edel
- Department of Chemistry, Imperial College London
- Beata Wojciak-Stothard
- National Heart and Lung Institute, Imperial College London
- DOI
- https://doi.org/10.1038/s42003-022-04169-z
- Journal volume & issue
-
Vol. 5,
no. 1
pp. 1 – 15
Abstract
A biomimetic inducible model of pulmonary arterial hypertension (PAH) is presented, combining natural and induced BMPR2 dysfunction with hypoxia in lung endothelial cells and blood-derived PAH cells to induce smooth muscle activation & proliferation.
