Evidence map›Paper›PMID 9065783›Full record

ArticleThe Biochemical journal1997

Regulation of platelet-activating factor receptor gene expression in vivo by endotoxin, platelet-activating factor and endogenous tumour necrosis factor.

H Wang, X Tan, H Chang, F Gonzalez-Crussi, D G Remick, W Hsueh

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 58 citations in OpenAlex.

  1. Effect of antiplatelet agents onFrontiers in microbiology · 2022
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Inflammatory signaling in NEC: Role of NF-κB, cytokines and other inflammatory mediators.Pathophysiology : the official journal of the International Society for Pathophysiology · 2014
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Probiotic and prebiotic supplementation for the prevention of neonatal necrotizing enterocolitis.Journal of perinatology : official journal of the California Perinatal Association · 2009
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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.

H WangDepartment of Pathology, Northwestern University, Chicago, IL 60614, U.S.A.
X Tan
H Chang
F Gonzalez-Crussi
D G Remick
W Hsueh
Northwestern Memorial Hospital · USUniversity of Michigan · US

Funding

PATHOGENESIS OF EXPERIMENTAL BOWEL NECROSISR01DK034574 · NIDDK · CHILDREN'S MEMORIAL HOSPITAL (CHICAGO) · PI HSUEH, WEI · 1986 to 2001
$421k
MOLECULAR MECHANISM OF EXPERIMENTAL INTESTINAL INJURYR01HD031840 · NICHD · CHILDREN'S MEMORIAL HOSPITAL (CHICAGO) · PI HSUEH, WEI · 1994 to 1998
–
NICHD NIH HHS HD31840NIDDK NIH HHS DK34574
6 · The paper itself

Abstract

A competitive PCR assay was developed to quantify platelet-activating factor (PAF) receptor (PAF-R) transcripts in rat tissues using a synthetic RNA as a competitor. We found PAF-R mRNA constitutively expressed in the eight organs tested, with the ileum containing the highest concentration [(3.49+/-0.15) x 10(7) molecules/microg of RNA]. Significant but lower levels were also detected in the jejunum, spleen, lungs, kidneys, heart, stomach and liver. Furthermore we defined the regulatory role of inflammatory mediators in ileal PAF-R gene expression using a rat model of intestinal injury induced by PAF or lipopolysaccharide (LPS). Injection of LPS or low-dose PAF resulted in a marked increase in ileal PAF-R mRNA within 30 min. The up-regulation on PAF-R elicited by PAF was biphasic, peaking first at 90 min, then again at 6 h. In contrast, LPS elicited a weak monophasic response. The second phase of PAF-R mRNA increase after PAF administration was completely abolished by WEB 2170, a PAF antagonist, and partially inhibited by antitumour necrosis factor (TNF) antibody. These observations indicate the involvement of endogenous PAF and TNF in this event. In conclusion, we found: (a) preferential PAF-R expression in the ileum, suggesting a role for PAF in intestinal inflammation; (b) induction of PAF-R expression in vivo by its own agonist; (c) a complex regulation of PAR-R gene expression in vivo involving a network of various pro-inflammatory mediators.

Indexed as

Receptors, Cell SurfaceReceptors, G-Protein-CoupledUp-RegulationAnimalsBlood PressureHematocritIleumIndomethacinLipopolysaccharidesMaleMutagenesis, Site-DirectedPlatelet Activating FactorPlatelet Membrane GlycoproteinsPolymerase Chain ReactionRatsRats, Sprague-DawleyIndomethacinLipopolysaccharidesPlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsReceptors, Cell SurfaceReceptors, G-Protein-CoupledRNA, ComplementaryRNA-Directed DNA PolymeraseRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID9065783
PMCPMC1218232
OpenAlexW206604000

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.