Evidence map›Paper›PMID 23859805›Full record

ArticleStem cell research2013

Loss of androgen receptor promotes adipogenesis but suppresses osteogenesis in bone marrow stromal cells.

Chiung-Kuei Huang, Kuo-Pao Lai, Jie Luo, Meng-Yin Tsai, Hong-Yo Kang, Yuhchyau Chen, Soo Ok Lee, Chawnshang Chang

Abstract read
In one paragraph

Article in Stem cell research, 2013. 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
1.0field-weighted citation impact, top 21% 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, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of the androgen receptor in the pathogenesis of obesity and its utility as a target for obesity treatments.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Alcohol-mediated miR-34a modulates hepatocyte growth and apoptosis.Journal of cellular and molecular medicine · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Sex steroid actions in male bone.Endocrine reviews · 2014
    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

8 authors at 3 institutions in 2 countries.

Chiung-Kuei HuangGeorge Whipple Lab for Cancer Research, Department of Pathology, and The Wilmot Cancer Center University of Rochester Medical Center, Rochester, NY 14642, USA.
Kuo-Pao Lai
Jie Luo
Meng-Yin Tsai
Hong-Yo Kang
Yuhchyau Chen
Soo Ok Lee
Chawnshang Chang
University of Rochester Medical Center · USChang Gung University · TWChina Medical University · TW

Funding

Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
Loss of Androgen Receptor Promotes Metastatic Prostate CancerR01CA122840 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2007 to 2011
$1.5M
NCI NIH HHS CA122840NCI NIH HHS CA156700NCI NIH HHS R01 CA122840NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Gender differences have been described in osteoporosis with females having a higher risk of osteoporosis than males. The differentiation of bone marrow stromal cells (BMSCs) into bone or fat is a critical step for osteoporosis. Here we demonstrated that loss of the androgen receptor (AR) in BMSCs suppressed osteogenesis but promoted adipogenesis. The mechanism dissection studies revealed that AR deficiency suppressed osteogenesis-related genes to inhibit osteoblast differentiation from BMSCs. Knockout of AR promoted adipogenesis of BMSCs via Akt activation through IGFBP3-mediated IGF signaling, and the 5' promoter assay and chromatin immunoprecipitation assays further proved that AR could modulate IGFBP3 expression at the transcriptional level. Finally, addition of IGF inhibitors successfully masked the AR deficiency-induced Akt activation, and inhibitions of Akt, IGF1, and IGF2 pathways reversed the AR depletion effects on the adipogenesis process. These results suggested that AR-mediated changes in IGFBP3 might modulate the IGF-Akt axis to regulate adipogenesis in BMSCs.

Indexed as

AdipogenesisAnimalsBone Marrow CellsCell DifferentiationCell Growth ProcessesFemaleGene Knockout TechniquesHumansMaleMiceOsteogenesisOsteoporosisReceptors, AndrogenSignal TransductionStromal CellsReceptors, Androgen

Identifiers

PMID23859805
PMCPMC3748723
OpenAlexW2146661168

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.