Evidence map›Paper›PMID 28342779›Full record

ArticleToxicology2017

Suppression of calpain expression by NSAIDs is associated with inhibition of cell migration in rat duodenum.

Kristopher Silver, A Littlejohn, Laurel Thomas, Bhupinder Bawa, James D Lillich

Abstract read
In one paragraph

Article in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Polysaccharides fromJournal of ginseng research · 2023
    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

5 authors at 1 institution in 1 country.

Kristopher SilverAnatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA. Electronic address: ksilver@ksu.edu.
A LittlejohnAnatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA.
Laurel ThomasAnatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA.
Bhupinder BawaDiagnostic Medicine and Pathobiology, Kansas State University, Manhattan, KS 66506, USA.
James D LillichAnatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA.
Kansas State University · US

Funding

Novel Mechanisms of NSAID-induced GI ToxicityR15DK091791 · NIDDK · KANSAS STATE UNIVERSITY · PI LILLICH, JAMES D · 2012 to 2012
$333k
NIDDK NIH HHS R15 DK091791
6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for the alleviation of pain and inflammation, but these drugs are also associated with a suite of negative side effects. Gastrointestinal (GI) toxicity is particularly concerning since it affects an estimated 70% of individuals taking NSAIDs routinely, and evidence suggests the majority of toxicity is occurring in the small intestine. Traditionally, NSAID-induced GI toxicity has been associated with indiscriminate inhibition of cyclooxygenase isoforms, but other mechanisms, including inhibition of cell migration, intestinal restitution, and wound healing, are likely to contribute to toxicity. Previous efforts demonstrated that treatment of cultured intestinal epithelial cells (IEC) with NSAIDs inhibits expression and activity of calpain proteases, but the effects of specific inhibition of calpain expression in vitro or the effects of NSAIDs on intestinal cell migration in vivo remain to be determined. Accordingly, we examined the effect of suppression of calpain protease expression with siRNA on cell migration in cultured IECs and evaluated the effects of NSAID treatment on epithelial cell migration and calpain protease expression in rat duodenum. Our results show that calpain siRNA inhibits protease expression and slows migration in cultured IECs. Additionally, NSAID treatment of rats slowed migration up the villus axis and suppressed calpain expression in duodenal epithelial cells. Our results are supportive of the hypothesis that suppression of calpain expression leading to slowing of cell migration is a potential mechanism through which NSAIDs cause GI toxicity.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCalpainCell LineCell MovementDuodenumEpithelial CellsIndomethacinIntestinal MucosaMaleNitrobenzenesRats, WistarRNA, Small InterferingSulfonamidesAnti-Inflammatory Agents, Non-SteroidalCalpainCapn1 protein, ratCapn2 protein, ratIndomethacinN-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNitrobenzenesRNA, Small InterferingSulfonamidesBromodeoxyuridineCalpainCell migration inhibitionDuodenumNsaid

Identifiers

PMID28342779
PMCPMC5519291
OpenAlexW2601846720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.