PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD+ levels and increasing SIRT1 activity.

Abstract:

BACKGROUND:Nicotinamide adenine dinucleotide (NAD+) is a critical molecule involved in various biological functions. Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD+ levels and play essential roles in regulating metabolism. However, there has been little research on the effects of PARP1 and SIRT1 crosstalk during senescence. METHODS:We isolated endothelial progenitor cells (EPCs) from human umbilical cord blood and treated them with a PARP1 inhibitor (PJ34). RESULTS:Using a stress-induced premature aging model built by H2O2, transfection with adenoviral vectors, and Western blot analysis, we observed that PJ34 treatment preserved intracellular NAD+ levels, increased SIRT1 activity, decreased p53 acetylation, and improved the function of stress-induced premature aging EPCs. CONCLUSIONS:Our results suggest that PJ34 improves the function of aging-induced EPCs and may contribute to cellular therapies for atherosclerosis.

journal_name

Stem Cell Res Ther

authors

Zha S,Li Z,Cao Q,Wang F,Liu F

doi

10.1186/s13287-018-0961-7

subject

Has Abstract

pub_date

2018-08-23 00:00:00

pages

224

issue

1

issn

1757-6512

pii

10.1186/s13287-018-0961-7

journal_volume

9

pub_type

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