Evidence map›Paper›PMID 20200986›Full record

ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2010

A role for ethanol-induced oxidative stress in controlling lineage commitment of mesenchymal stromal cells through inhibition of Wnt/beta-catenin signaling.

Jin-Ran Chen, Oxana P Lazarenko, Kartik Shankar, Michael L Blackburn, Thomas M Badger, Martin J Ronis

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. [Progress of pathogenesis and genetics of alcohol-induced osteonecrosis of femoral head].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022
    Review
  11. Article
  12. Article
  13. Pharmacogenomics and personalized medicine · 2022
    Article
  14. Oxidative Stress and Ginsenosides: An Update on the Molecular Mechanisms.Oxidative medicine and cellular longevity · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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.

Jin-Ran ChenArkansas Children's Nutrition Center, 15 Children's Way, Little Rock, AR 72202, USA. chenjinran@uams.edu
Oxana P Lazarenko
Kartik Shankar
Michael L Blackburn
Thomas M Badger
Martin J Ronis
Arkansas Children's Nutrition Center · USArkansas Department of Agriculture · US

Funding

Alcohol-Induced Bone Resorption: The Role of Oxidative StressR01AA018282 · NIAAA · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI RONIS, MARTIN J J · 2009 to 2013
$1.7M
ETHANOL EFFECTS ON BONE FORMATION IN PREGNANCYR01AA012928 · NIAAA · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI RONIS, MARTIN J.J. · 2002 to 2006
$1.4M
NIAAA NIH HHS R01 AA012928NIAAA NIH HHS R01 AA018282NIAAA NIH HHS R01 AA12928NIAAA NIH HHS R01 AA18282
6 · The paper itself

Abstract

The mechanisms by which chronic ethanol intake induces bone loss remain unclear. In females, the skeletal response to ethanol varies depending on physiologic status (e.g., cycling, pregnancy, or lactation). Ethanol-induced oxidative stress appears to be a key event leading to skeletal toxicity. In this study, ethanol-containing liquid diets were fed to postlactational female Sprague-Dawley rats intragastrically for 4 weeks beginning at weaning. Ethanol consumption decreased bone mineral density (BMD) compared with control animals during this period of bone rebuilding following the end of lactation. Coadministration of the antioxidant N-acetylcysteine (NAC) was able to block bone loss and downregulation of the bone-formation markers alkaline phosphatase and osteocalcin in serum and gene expression in bone. Real-time array analysis of total RNA isolated from bone tissue revealed that the majority of Wnt signaling components were downregulated by chronic ethanol infusion. Real-time PCR confirmed downregulated gene expression in a subset of the Wnt signaling components by ethanol. However, the Wnt antagonist DKK1 was upregulated by ethanol. The key canonical Wnt signaling molecule beta-catenin protein expression was inhibited, while glycogen synthase kinase-3-beta was dephosphorylated by ethanol in bone and preosteoblastic cells. These actions of ethanol were blocked by NAC. Ethanol treatment inactivated TCF/LEF gene transcription, eliminated beta-catenin nuclear translocation in osteoblasts, and reciprocally suppressed osteoblastogenesis and enhanced adipogenesis. These effects of ethanol on lineage commitment of mesenchymal stem cells were eliminated by NAC pretreatment. These observations are consistent with the hypothesis that ethanol inhibits bone formation through stimulation of oxidative stress to suppress Wnt signaling.

Indexed as

Oxidative StressAcetylcysteineAdipogenesisAnimalsbeta CateninBone DensityCell DifferentiationCell LineageDown-RegulationEthanolFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaLactationMesenchymal Stem CellsOsteogenesisAcetylcysteinebeta CateninEthanolGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaTCF Transcription FactorsWnt Proteins

Identifiers

PMID20200986
PMCPMC3153370
OpenAlexW2068659212

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.