ArticleThe Journal of biological chemistry2016
Transcriptional Reprogramming and Resistance to Colonic Mucosal Injury in Poly(ADP-ribose) Polymerase 1 (PARP1)-deficient Mice.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05561738 (Nicotinamide Riboside in Ulcerative Colitis), which is not on this map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Nicotinamide Riboside in Ulcerative Colitis
Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Excessive poly(ADP)-ribosylation in the inflamed mucosa of pediatric celiac disease points to a novel inflammatory mechanism and therapeutic target.Molecular and cellular pediatrics · 2026Article
- Knockout of PARP2 in T cells leads to spontaneous colitis with distinct segmental characteristics in PARP1-deficient mice.Frontiers in immunology · 2026Article
- Combinatorial Effects of Cisplatin and PARP Inhibitor Olaparib on Survival, Intestinal Integrity, and Microbiome Modulation in Murine Model.International journal of molecular sciences · 2025Article
- Specific and shared biological functions of PARP2 - is PARP2 really a lil' brother of PARP1?Expert reviews in molecular medicine · 2024Review
- NADAntioxidants (Basel, Switzerland) · 2023Review
- Transcriptomic Analysis of CRISPR/Cas9-Mediated PARP1-Knockout Cells under the Influence of Topotecan and TDP1 Inhibitor.International journal of molecular sciences · 2023Article
- PARP1 Gene Knockout Suppresses Expression of DNA Base Excision Repair Genes.Doklady. Biochemistry and biophysics · 2023Article
- Epithelial NADFrontiers in immunology · 2023Article
- NADTrends in immunology · 2022Review
- PARkinson's: From cellular mechanisms to potential therapeutics.Pharmacology & therapeutics · 2022Review
- Reduced Colonic Mucosal Injury in 2,3,7,8-Tetrachlorodibenzo-International journal of molecular sciences · 2022Article
- Metabolic analyses reveal dysregulated NAD+ metabolism and altered mitochondrial state in ulcerative colitis.PloS one · 2022Article
- Review
- An integrative drug repositioning framework discovered a potential therapeutic agent targeting COVID-19.Signal transduction and targeted therapy · 2021Article
- The role of the microbiome in ovarian cancer: mechanistic insights into oncobiosis and to bacterial metabolite signaling.Molecular medicine (Cambridge, Mass.) · 2021Review
- Poly(ADP-ribose) polymerase-1 inhibitor ameliorates dextran sulfate sodium-induced colitis in mice by regulating the balance of Th17/Treg cells and inhibiting the NF-Experimental and therapeutic medicine · 2021Article
- Targeting PARP-1 with metronomic therapy modulates MDSC suppressive function and enhances anti-PD-1 immunotherapy in colon cancer.Journal for immunotherapy of cancer · 2021Article
- A comprehensive review on drug repositioning against coronavirus disease 2019 (COVID19).Naunyn-Schmiedeberg's archives of pharmacology · 2020Review
- The role of ADP-ribose metabolism in metabolic regulation, adipose tissue differentiation, and metabolism.Genes & development · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate and participate in the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator cytokines, chemokines, and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to determine the impact of Parp1 deletion on the innate immune response to mucosal injury and on the gut microbiome composition. Parp1 deficiency was evaluated in DSS-induced colitis in WT, Parp1(-/-), Rag2(-/-), and Rag2(-/-)×Parp1(-/-) double knock-out mice. Genome-wide analysis of the colonic transcriptome and fecal 16S amplicon profiling was performed. Compared with WT, we demonstrated that Parp1(-/-) were protected from dextran-sulfate sodium-induced colitis and that this protection was associated with a dramatic transcriptional reprogramming in the colon. PARP1 deficiency was also associated with a modulation of the colonic microbiota (increases relative abundance of Clostridia clusters IV and XIVa) and a concomitant increase in the frequency of mucosal CD4(+)CD25(+) Foxp3(+) regulatory T cells. The protective effects conferred by Parp1 deletion were lost in Rag2(-/-) × Parp1(-/-) mice, highlighting the role of the adaptive immune system for full protection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.