Nature Communications (Nov 2016)
PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia
- Roxana Ola,
- Alexandre Dubrac,
- Jinah Han,
- Feng Zhang,
- Jennifer S. Fang,
- Bruno Larrivée,
- Monica Lee,
- Ana A. Urarte,
- Jan R. Kraehling,
- Gael Genet,
- Karen K. Hirschi,
- William C. Sessa,
- Francesc V. Canals,
- Mariona Graupera,
- Minhong Yan,
- Lawrence H. Young,
- Paul S. Oh,
- Anne Eichmann
Affiliations
- Roxana Ola
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Alexandre Dubrac
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Jinah Han
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Feng Zhang
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Jennifer S. Fang
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Bruno Larrivée
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Monica Lee
- Department of Pharmacology, Yale University School of Medicine
- Ana A. Urarte
- Vascular Signalling Laboratory, Institut d’Investigació Biomèdica de Bellvitge, L’Hospitalet de Llobregat
- Jan R. Kraehling
- Department of Pharmacology, Yale University School of Medicine
- Gael Genet
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Karen K. Hirschi
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- William C. Sessa
- Department of Pharmacology, Yale University School of Medicine
- Francesc V. Canals
- Translation Research Laboratory, Catalan Institute of Oncology, Idibell
- Mariona Graupera
- Vascular Signalling Laboratory, Institut d’Investigació Biomèdica de Bellvitge, L’Hospitalet de Llobregat
- Minhong Yan
- Molecular Oncology, Genentech, Inc.
- Lawrence H. Young
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- Paul S. Oh
- Department of Physiology and Functional Genomics, University of Florida College of Medicine
- Anne Eichmann
- Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine
- DOI
- https://doi.org/10.1038/ncomms13650
- Journal volume & issue
-
Vol. 7,
no. 1
pp. 1 – 12
Abstract
Arteriovenous malformations (AVM) is a hallmark of hereditary haemorrhagic telangiectasia type 2, a disease caused by mutations in BMP receptor ALK1. Ola et al. show that AVM can be caused by blocking BMP9 and BMP10 in mice, leading to increased VEGF and PI3K activity, and that pharmacologic inhibition of PI3K prevents AVM development.
