Human venous valve disease caused by mutations in FOXC2 and GJC2

Venous valves (VVs) prevent venous hypertension and ulceration. We report that FOXC2 and GJC2 mutations are associated with reduced VV number and length. In mice, early VV formation is marked by elongation and reorientation (“organization”) of Prox1(hi) endothelial cells by postnatal day 0. The expr...

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Detalhes bibliográficos
Publicado no:J Exp Med
Main Authors: Lyons, Oliver, Saha, Prakash, Seet, Christopher, Kuchta, Adam, Arnold, Andrew, Grover, Steven, Rashbrook, Victoria, Sabine, Amélie, Vizcay-Barrena, Gema, Patel, Ash, Ludwinski, Francesca, Padayachee, Soundrie, Kume, Tsutomu, Kwak, Brenda R., Brice, Glen, Mansour, Sahar, Ostergaard, Pia, Mortimer, Peter, Jeffery, Steve, Brown, Nigel, Makinen, Taija, Petrova, Tatiana V., Modarai, Bijan, Smith, Alberto
Formato: Artigo
Idioma:Inglês
Publicado em: The Rockefeller University Press 2017
Assuntos:
Research Articles
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC5551565/
https://ncbi.nlm.nih.gov/pubmed/28724617
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1084/jem.20160875
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