New Journal of Science / 2014 / Article / Tab 2

Review Article

Regulation of EPCs: The Gateway to Blood Vessel Formation

Table 2

EPC derived from cellular reprogramming.

iPS cellsIVPCsSK-1Epigenetic modification

Starting cell typeMouse/human embryonic fibroblasts, ECFCsRat ECsHUVECMurine and human EPCs

InterventionRetroviral transduction of Oct4, Sox2, Klf4, c-MycLentiviral transduction of Oct4, Sox2, Klf4, c-MycLentiviral transduction of SK-1Inhibitors of DNA methyltransferases (5-azacytidine), histone deacetylases (valproic acid), G9a histone dimethyl-transferase (BIX-01294)

DedifferentiationFullPartialPartialPartial

PhenotypeAlkaline Phosphatase, Sox2, Oct3/4, Nanog
High E-cadherin
Low E-cadherinCD34, CD133, CD117 
Nanog 
CD144, CD31, vWF
Enhanced global transcription 
Oct-4, Nanog, Sox2 
eNOS, CD144

In vitro functionProliferation
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 functionForm teratomasImprove 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

References[137139][141][44, 83][143]

iPS: induced pluripotent; iVPC: induced vascular progenitor cells; SK-1: sphingosine kinase-1; HUVEC: human umbilical vein endothelial cell; MI: myocardial infarction.

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