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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Pubblicato in:J Exp Med
Autori principali: 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
Natura: Artigo
Lingua:Inglês
Pubblicazione: The Rockefeller University Press 2017
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Research Articles
Accesso online: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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