Evidence map›Paper›PMID 18181150›Full record

ArticleJournal of cellular physiology2008

The anti-apoptosis protein, survivin, mediates gastric epithelial cell cytoprotection against ethanol-induced injury via activation of the p34(cdc2) cyclin-dependent kinase.

Michael K Jones, Oscar R Padilla, Nicole A Webb, Manith Norng

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Prognostic Significance of p27 and Survivin in H. pylori Gastritis and Gastric Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021
    Article
  4. Article
  5. Article
  6. Ghrelin inhibition of ethanol-induced gastric epithelial cell apoptosis is mediated by miR-21.International journal of clinical and experimental pathology · 2015
    Article
  7. Article
  8. Article
  9. Article
  10. Alcohol exposure and mechanisms of tissue injury and repair.Alcoholism, clinical and experimental research · 2011
    Review
  11. Article
  12. Article
  13. Survivin is a key factor in the differential susceptibility of gastric endothelial and epithelial cells to alcohol-induced injury.Journal of physiology and pharmacology : an official journal of the Polish Physiological Society · 2010
    Article
  14. Article
  15. Gastroduodenal mucosal defense.Current gastroenterology reports · 2008
    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

4 authors at 1 institution in 1 country.

Michael K JonesResearch, Veterans Affairs Long Beach Healthcare System, Long Beach, California 90822, USA. michael.jones4@med.va.gov
Oscar R Padilla
Nicole A Webb
Manith Norng
VA Long Beach Healthcare System · US

Funding

Alcohol Injury Healing, Cytoprotection and SurvivinR01AA014946 · NIAAA · SOUTHERN CALIFORNIA INST FOR RES/EDUC · PI JONES, MICHAEL K · 2005 to 2009
$1.1M
NIAAA NIH HHS 5R01AA014946-03NIAAA NIH HHS R01 AA014946
6 · The paper itself

Abstract

The anti-apoptosis protein, survivin, promotes cell survival and mitosis. Recent studies have demonstrated that survivin is expressed in normal gastric mucosa. Using an in vitro model, we examined whether survivin plays a role in the cytoprotection produced in gastric mucosa by mild irritant ethanol (ETOH) against subsequent exposure to concentrated ETOH. Pre-treatment of rat gastric epithelial cells with 1% ETOH reduced cell death, in response to subsequent incubation with 5% ETOH, by 94% (P < 0.005). This pre-treatment also resulted in increased total and phosphorylated survivin protein levels by 180% (P < 0.0001) and 540% (P < 0.0002), respectively, which required the p34(cdc2) cell cycle-dependent kinase. The cytoprotective effect was abrogated upon siRNA knockdown of survivin protein levels. Further, overexpression of exogenous survivin resulted in significant cytoprotection by 62% (P < 0.02) in the absence of any pre-treatment. We further examined the in vivo relevance of these findings. In fasted rats, administration of 20% ETOH, which we found to be 93% (P < 0.0001) cytoprotective against 50% ETOH challenge, resulted in increased total and phosphorylated survivin protein levels by 234% (P < 0.001) and 214% (P < 0.02), respectively. Administration of 20% ETOH resulted in increased gastric p34(cdc2) activity by 146% (P < 0.01). Inhibition of p34(cdc2) by the potent inhibitor, roscovitine, abolished the increased survivin levels in response to pre-administration of 20% ETOH and reduced the cytoprotection against 50% ETOH challenge by 59% (P < 0.01). These results indicate that survivin is a key mediator of cytoprotection against ETOH-induced gastric injury, acting at the epithelial cell level, by a mechanism that is dependent, in part, on p34(cdc2).

Indexed as

ApoptosisAnimalsCDC2 Protein KinaseCytoprotectionEnzyme ActivationEpithelial CellsEthanolGastric MucosaMaleMicrotubule-Associated ProteinsPhosphoproteinsProtein BiosynthesisRatsRats, Sprague-DawleyRNA, MessengerStomachBirc5 protein, ratCDC2 Protein KinaseEthanolMicrotubule-Associated ProteinsPhosphoproteinsRNA, MessengerSurvivinThreonine

Identifiers

PMID18181150
PMCPMC2288653
OpenAlexW2026976911

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.