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ROBO4 variants predispose individuals to bicuspid aortic valve and thoracic aortic aneurysm
Journal article   Open access   Peer reviewed

ROBO4 variants predispose individuals to bicuspid aortic valve and thoracic aortic aneurysm

Russell A Gould, Hamza Aziz, Courtney E Woods, Manuel Alejandro Seman-Senderos, Elizabeth Sparks, Christoph Preuss, Florian Wünnemann, Djahida Bedja, Cassandra R Moats, Sarah A McClymont, …
Nature genetics, v 51(1), pp 42-50
01 Jan 2019
PMID: 30455415
url
https://europepmc.org/articles/pmc6309588View
Accepted (AM) Open
url
https://doi.org/10.1038/s41588-018-0265-yView
Published, Version of Record (VoR) Open

Abstract

Animals Aortic Aneurysm, Thoracic - genetics Aortic Valve - abnormalities Bicuspid Aortic Valve Disease Cells, Cultured Disease Models, Animal Endothelial Cells - physiology Female Heart Valve Diseases - genetics Humans Male Mice Mice, Inbred C57BL Mice, Knockout Mutation - genetics Phenotype Receptors, Cell Surface - genetics Zebrafish
Bicuspid aortic valve (BAV) is a common congenital heart defect (population incidence, 1-2%) that frequently presents with ascending aortic aneurysm (AscAA) . BAV/AscAA shows autosomal dominant inheritance with incomplete penetrance and male predominance. Causative gene mutations (for example, NOTCH1, SMAD6) are known for ≤1% of nonsyndromic BAV cases with and without AscAA , impeding mechanistic insight and development of therapeutic strategies. Here, we report the identification of variants in ROBO4 (which encodes a factor known to contribute to endothelial performance) that segregate with disease in two families. Targeted sequencing of ROBO4 showed enrichment for rare variants in BAV/AscAA probands compared with controls. Targeted silencing of ROBO4 or mutant ROBO4 expression in endothelial cell lines results in impaired barrier function and a synthetic repertoire suggestive of endothelial-to-mesenchymal transition. This is consistent with BAV/AscAA-associated findings in patients and in animal models deficient for ROBO4. These data identify a novel endothelial etiology for this common human disease phenotype.

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Web of Science research areas
Genetics & Heredity
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