We are analyzing https://link.springer.com/article/10.1186/s13287-018-0961-7.

Title:
PARP1 inhibitor (PJ34) improves the function of aging-induced endothelial progenitor cells by preserving intracellular NAD+ levels and increasing SIRT1 activity | Stem Cell Research & Therapy
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 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.
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Keywords {🔍}

cells, sirt, epcs, article, parp, nad, aging, senescence, cell, levels, google, scholar, endothelial, cas, fig, effects, treatment, expression, cellular, par, activity, intracellular, treated, increased, protein, poly, adpribose, blood, function, progenitor, results, medium, western, blot, epc, senescent, research, polymerase, sirtuin, decreased, ability, control, saβgal, human, study, acp, incubated, versus, atherosclerosis, migration,

Topics {✒️}

positive feedback loop ischemic post-conditioning-induced cardioprotection 10 μm dichloro-dihydro-fluorescein diacetate sa-β-gal positivity increased mesenchymal stem cells sa-β-gal staining kit age-related diseases doxorubicin-induced premature senescence sa-β-gal assays mecp2-mediated epigenetic regulation oxidative stress-induced aging fluorescence enzyme-labeling device sa-β-gal activity article download pdf sa1/sa2 cohesion proteins anti-β-actin antibody sirt1 short-hairpin rna nad/nadh assay kit reactive oxygen species positive expression rates sirtuin1-p53 regulatory axis nicotinamide adenine dinucleotide neuron death mediated mecp2 mediated dysfunction measure nad/nadh levels sa-β-gal full access anti-rabbit secondary antibodies redox-sensitive protein involved cell counting kit related subjects von willebrand factor endothelial progenitor cells aging-related impairment 200 μl serum-free medium human endothelial cells privacy choices/manage cookies oxidative stress responses sublethal oxidative stress lethal oxidative stress measure cellular ros epc endothelial markers endothelial cell senescence identify cellular senescence pathological dna damage heat-shock stress increased ac-p53 activity increasing sirt1 activity fang liu creative commons license

Questions {❓}

Soft tissue sarcomas: new opportunity of treatment with PARP inhibitors?

Schema {🗺️}

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         description: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. We isolated endothelial progenitor cells (EPCs) from human umbilical cord blood and treated them with a PARP1 inhibitor (PJ34). 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. Our results suggest that PJ34 improves the function of aging-induced EPCs and may contribute to cellular therapies for atherosclerosis.
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