Abstract：
:ETS transcription factors ETV2, FLI1, and ERG1 specify pluripotent stem cells into induced vascular endothelial cells (iVECs). However, iVECs are unstable and drift toward nonvascular cells. We show that human midgestation c-Kit(-) lineage-committed amniotic cells (ACs) can be reprogrammed into vascular endothelial cells (rAC-VECs) without transitioning through a pluripotent state. Transient ETV2 expression in ACs generates immature rAC-VECs, whereas coexpression with FLI1/ERG1 endows rAC-VECs with a vascular repertoire and morphology matching mature endothelial cells (ECs). Brief TGFβ-inhibition functionalizes VEGFR2 signaling, augmenting specification of ACs into rAC-VECs. Genome-wide transcriptional analyses showed that rAC-VECs are similar to adult ECs in which vascular-specific genes are expressed and nonvascular genes are silenced. Functionally, rAC-VECs form stable vasculature in Matrigel plugs and regenerating livers. Therefore, short-term ETV2 expression and TGFβ inhibition with constitutive ERG1/FLI1 coexpression reprogram mature ACs into durable rAC-VECs with clinical-scale expansion potential. Banking of HLA-typed rAC-VECs establishes a vascular inventory for treatment of diverse disorders.
journal_name
Celljournal_title
Cellauthors
Ginsberg M,James D,Ding BS,Nolan D,Geng F,Butler JM,Schachterle W,Pulijaal VR,Mathew S,Chasen ST,Xiang J,Rosenwaks Z,Shido K,Elemento O,Rabbany SY,Rafii Sdoi
10.1016/j.cell.2012.09.032subject
Has Abstractpub_date
2012-10-26 00:00:00pages
559-75issue
3eissn
0092-8674issn
1097-4172pii
S0092-8674(12)01178-6journal_volume
151pub_type
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