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Efficient direct reprogramming of mature amniotic cells into endothelial cells by ETS factors and TGFβ suppression. | LitMetric

AI Article Synopsis

  • Researchers found that certain transcription factors (ETV2, FLI1, ERG1) can reprogram specific amniotic cells into stable vascular endothelial cells (rAC-VECs) without needing to go through a pluripotent stage.
  • The process involves temporarily expressing ETV2 and combining it with FLI1 and ERG1, which leads to the development of mature cells that have the characteristics of adult endothelial cells and can form stable blood vessels.
  • By inhibiting TGFβ signaling, the efficiency of this reprogramming is increased, allowing for potential clinical applications, such as creating a bank of HLA-typed rAC-VECs for treating various vascular disorders.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507451PMC
http://dx.doi.org/10.1016/j.cell.2012.09.032DOI Listing

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