Evidence map›Paper›PMID 15554929›Full record

ArticleImmunology2004

Activator protein-1 signalling pathway and apoptosis are modulated by poly(ADP-ribose) polymerase-1 in experimental colitis.

Basilia Zingarelli, Paul W Hake, Timothy J Burroughs, Giovanna Piraino, Michael O'connor, Alvin Denenberg

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Epithelial NADFrontiers in immunology · 2023
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Novel insights into PARPs in gene expression: regulation of RNA metabolism.Cellular and molecular life sciences : CMLS · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Basilia ZingarelliDivision of Critical Care Medicine, Cincinnati Children's Hospital Medical Center and College of Medicine, University of Cincinnati, Cincinnati, OH 45229, USA. basilia.zingarelli@cchmc.org
Paul W Hake
Timothy J Burroughs
Giovanna Piraino
Michael O'connor
Alvin Denenberg
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) is activated in response to DNA injury in the nucleus of eukaryotic cells and has been implicated in intestinal barrier dysfunction during inflammatory bowel diseases. In this study we investigated whether PARP-1 may regulate the inflammatory response of experimental colitis at the level of signal transduction mechanisms. Mice genetically deficient of PARP-1 (PARP-1(-/-)) and wild-type littermates were subjected to rectal instillation of trinitrobenzene sulphonic acid (TNBS). Signs of inflammation were monitored for 14 days. In wild-type mice, TNBS treatment resulted in colonic ulceration and marked apoptosis, which was associated with decreased colon content of the antiapoptotic protein Bcl-2, whereas the proapoptotic Bax was unchanged. Elevated levels of plasma nitrate/nitrite, metabolites of nitric oxide (NO), were also found. These inflammatory events were associated with activation of c-Jun-NH(2) terminal kinase (JNK), phosphorylation of c-Jun and activation of the nuclear transcription factor activator protein-1 (AP-1) in the colon. In contrast, PARP-1(-/-) mice exhibited a significant reduction of colon damage and apoptosis, which was associated with increased colonic expression of Bcl-2 and lower levels of plasma nitrate/nitrite when compared to wild-type mice. Amelioration of colon damage was associated with a significant reduction of the activation of JNK and reduction of the DNA binding of AP-1. The data indicate that PARP-1 exerts a pathological role in colitis possibly by regulating the early stress-related transcriptional response through a positive modulation of the AP-1 and JNK pathways.

Indexed as

ApoptosisAnimalsbcl-2-Associated X ProteinColitisJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4MiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase KinasesNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIPhosphorylationPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesBax protein, mousebcl-2-Associated X ProteinJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Mitogen-Activated Protein Kinase KinasesNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Transcription Factor AP-1

Identifiers

PMID15554929
PMCPMC1782595
OpenAlexW2037746176

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.