CRISPR/Cas9-mediated gene knockout reveals a guardian role of NF-κB/RelA in maintaining the homeostasis of human vascular cells

Protein Cell. 2018 Nov;9(11):945-965. doi: 10.1007/s13238-018-0560-5. Epub 2018 Jul 2.

Abstract

Vascular cell functionality is critical to blood vessel homeostasis. Constitutive NF-κB activation in vascular cells results in chronic vascular inflammation, leading to various cardiovascular diseases. However, how NF-κB regulates human blood vessel homeostasis remains largely elusive. Here, using CRISPR/Cas9-mediated gene editing, we generated RelA knockout human embryonic stem cells (hESCs) and differentiated them into various vascular cell derivatives to study how NF-κB modulates human vascular cells under basal and inflammatory conditions. Multi-dimensional phenotypic assessments and transcriptomic analyses revealed that RelA deficiency affected vascular cells via modulating inflammation, survival, vasculogenesis, cell differentiation and extracellular matrix organization in a cell type-specific manner under basal condition, and that RelA protected vascular cells against apoptosis and modulated vascular inflammatory response upon tumor necrosis factor α (TNFα) stimulation. Lastly, further evaluation of gene expression patterns in IκBα knockout vascular cells demonstrated that IκBα acted largely independent of RelA signaling. Taken together, our data reveal a protective role of NF-κB/RelA in modulating human blood vessel homeostasis and map the human vascular transcriptomic landscapes for the discovery of novel therapeutic targets.

Keywords: Apoptosis; Inflammation; NF-κB; RelA; Stem cell.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Vessels / cytology*
  • Blood Vessels / metabolism
  • CRISPR-Cas Systems*
  • Embryonic Stem Cells / cytology
  • Gene Knockout Techniques*
  • Homeostasis*
  • Humans
  • NF-kappa B / deficiency
  • NF-kappa B / metabolism*
  • Transcription Factor RelA / deficiency
  • Transcription Factor RelA / metabolism*

Substances

  • NF-kappa B
  • RELA protein, human
  • Transcription Factor RelA