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

Authors :: Zha S
Li Z
Cao Q
Wang F
Liu F
Source :: Stem cell research & therapy [Stem Cell Res Ther] 2018 Aug 23; Vol. 9 (1), pp. 224. Date of Electronic Publication: 2018 Aug 23.
Publication Year :: 2018
Abstract: Background: Nicotinamide adenine dinucleotide (NAD <superscript>+</superscript> ) is a critical molecule involved in various biological functions. Poly (ADP-ribose) polymerase 1 (PARP1) and sirtuin 1 (SIRT1) affect cellular NAD <superscript>+</superscript> levels and play essential roles in regulating metabolism. However, there has been little research on the effects of PARP1 and SIRT1 crosstalk during senescence.<br />Methods: We isolated endothelial progenitor cells (EPCs) from human umbilical cord blood and treated them with a PARP1 inhibitor (PJ34).<br />Results: Using a stress-induced premature aging model built by H <subscript>2</subscript> O <subscript>2</subscript> , transfection with adenoviral vectors, and Western blot analysis, we observed that PJ34 treatment preserved intracellular NAD <superscript>+</superscript> levels, increased SIRT1 activity, decreased p53 acetylation, and improved the function of stress-induced premature aging EPCs.<br />Conclusions: Our results suggest that PJ34 improves the function of aging-induced EPCs and may contribute to cellular therapies for atherosclerosis.

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