Regulation of EPCs: The Gateway to Blood Vessel Formation
Table 2
EPC derived from cellular reprogramming.
iPS cells
IVPCs
SK-1
Epigenetic modification
Starting cell type
Mouse/human embryonic fibroblasts, ECFCs
Rat ECs
HUVEC
Murine and human EPCs
Intervention
Retroviral transduction of Oct4, Sox2, Klf4, c-Myc
Lentiviral transduction of Oct4, Sox2, Klf4, c-Myc
Lentiviral transduction of SK-1
Inhibitors of DNA methyltransferases (5-azacytidine), histone deacetylases (valproic acid), G9a histone dimethyl-transferase (BIX-01294)
Dedifferentiation
Full
Partial
Partial
Partial
Phenotype
Alkaline Phosphatase, Sox2, Oct3/4, Nanog High E-cadherin
Low E-cadherin
CD34, CD133, CD117 Nanog CD144, CD31, vWF
Enhanced global transcription Oct-4, Nanog, Sox2 eNOS, CD144
In vitro function
Proliferation Form embryoid bodies Can differentiate into neural and cardiac cells
Form tubes in vitro Align to flow Differentiate into ECs in response to VEGF
Ac-LDL uptake in vitro tube formation
In vivo function
Form teratomas
Improve coronary artery flow and cardiac function in a repeated MI model Do not form teratomas
Treated EPCs improved ejection fraction, left ventricular function; reduced infarct size, left ventricular fibrosis in a MI model Do not form teratomas