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PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity
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 researc...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6107962/ https://www.ncbi.nlm.nih.gov/pubmed/30139380 http://dx.doi.org/10.1186/s13287-018-0961-7 |
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author | Zha, Siyuan Li, Zhen Cao, Qing Wang, Fei Liu, Fang |
author_facet | Zha, Siyuan Li, Zhen Cao, Qing Wang, Fei Liu, Fang |
author_sort | Zha, Siyuan |
collection | PubMed |
description | 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 H(2)O(2), 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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13287-018-0961-7) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6107962 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-61079622018-08-29 PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity Zha, Siyuan Li, Zhen Cao, Qing Wang, Fei Liu, Fang Stem Cell Res Ther Research 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 H(2)O(2), 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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13287-018-0961-7) contains supplementary material, which is available to authorized users. BioMed Central 2018-08-23 /pmc/articles/PMC6107962/ /pubmed/30139380 http://dx.doi.org/10.1186/s13287-018-0961-7 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zha, Siyuan Li, Zhen Cao, Qing Wang, Fei Liu, Fang PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title | PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title_full | PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title_fullStr | PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title_full_unstemmed | PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title_short | PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD(+) levels and increasing SIRT1 activity |
title_sort | parp1 inhibitor (pj34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular nad(+) levels and increasing sirt1 activity |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6107962/ https://www.ncbi.nlm.nih.gov/pubmed/30139380 http://dx.doi.org/10.1186/s13287-018-0961-7 |
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