A role for the long non-coding RNA SENCR in commitment and function of endothelial cells

Mounia Boulberdaa, Scott Elizabeth, Ballantyne Margaret , Garcia Raquel , Betty Descamps , Gianni D Angelini, Mairi Brittan, Amanda L Hunter, Martin W. Mcbride, John D. Mcclure, Joseph M Miano , Costanza Emanueli, Nicholas Mills, Joanne C Mountford, Andrew Baker

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Despite the increasing importance of long non-coding RNA in physiology and disease, their role in endothelial biology remains poorly understood. Growing evidence has highlighted them to be essential regulators of human embryonic stem cell differentiation. SENCR, a vascular-enriched long non-coding RNA, overlaps the Friend Leukemia Integration virus 1 (FLI1) gene, a regulator of endothelial development. Therefore, we wanted to test the hypothesis that SENCR may contribute to mesodermal and endothelial commitment as well as in endothelial function. We thus developed new differentiation protocols allowing generation of endothelial cells from human embryonic stem cells using both directed and haemogenic routes. The expression of SENCR was markedly regulated during endothelial commitment using both protocols. SENCR did not control the pluripotency of pluripotent cells; however its overexpression significantly potentiated early mesodermal and endothelial commitment. In HUVEC, SENCR induced proliferation, migration and angiogenesis. SENCR expression was altered in vascular tissue and cells derived from patients with critical limb ischemia and premature coronary artery disease compared to controls. Here, we showed that SENCR contributes to the regulation of endothelial differentiation from pluripotent cells and controls the angiogenic capacity of HUVEC. These data give novel insight into the regulatory processes involved in endothelial development and function.
Original languageEnglish
JournalMolecular Therapy
Early online date5 Apr 2016
Publication statusE-pub ahead of print - 5 Apr 2016


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