Evidence map›Paper›PMID 24948012›Full record

ArticleCell death and differentiation2014

A novel PPARγ2 modulator sLZIP controls the balance between adipogenesis and osteogenesis during mesenchymal stem cell differentiation.

J Kim, J Ko

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Mesenchymal Stem Cells and Their Exocytotic Vesicles.International journal of molecular sciences · 2023
    Review
  11. Mesenchymal Stem Cell Senescence and Osteogenesis.Medicina (Kaunas, Lithuania) · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. mMolecular therapy. Nucleic acids · 2020
    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

2 authors at 1 institution in 1 country.

J KimDivision of Life Sciences, Korea University, Seoul 136-701, Korea.
J KoDivision of Life Sciences, Korea University, Seoul 136-701, Korea.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs), also known as multipotent stromal cells, are used in clinical trials. However, the use of MSCs for medical treatment of patients poses a potential problem due to the possibility of transdifferentiation into unwanted tissues. Disruption of the balance during MSC differentiation leads to obesity, skeletal fragility, and osteoporosis. Differentiation of MSCs into either adipocytes or osteoblasts is transcriptionally regulated by the two key transcription factors PPARγ2 and Runx2. PPARγ2 is highly expressed during adipocyte differentiation and regulates expression of genes involved in adipogenesis. Runx2 induces osteogenic gene expression and, thereby, increases osteoblast differentiation. Although transcriptional modulation of PPARγ2 has been investigated in adipogenesis, the underlying molecular mechanisms to control the balance between adipogenesis and osteogenesis in MSCs remain unclear. In this study, the role of sLZIP in regulation of PPARγ2 transcriptional activation was investigated along with sLZIP's involvement in differentiation of MSCs into adipocytes and osteoblasts. sLZIP interacts with PPARγ2 and functions as a corepressor of PPARγ2. sLZIP enhances formation of the PPARγ2 corepressor complex through specific interaction with HDAC3, resulting in suppression of PPARγ2 transcriptional activity. We found that sLZIP prevents expression of PPARγ2 target genes and adipocyte differentiation both in vitro and in vivo. sLZIP also upregulates Runx2 transcriptional activity via inhibition of PPARγ2 activity, and promotes osteoblast differentiation. sLZIP transgenic mice exhibited enhanced bone mass and density, compared with wild-type mice. These results indicate that sLZIP has a critical role in the regulation of osteogenesis and bone development. However, sLZIP does not affect chondrogenesis and osteoclastogenesis. We propose that sLZIP is a novel PPARγ2 modulator for control of the balance between adipogenesis and osteogenesis during MSC differentiation, and that sLZIP can be used as a therapeutic target molecule for treatment of obesity, osteodystrophy, and osteoporosis.

Indexed as

AdipocytesAdipogenesisAnimalsBone DensityCells, CulturedChondrogenesisCore Binding Factor Alpha 1 SubunitCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsEnhancer Elements, GeneticFatty Acid-Binding ProteinsHistone Deacetylase 3Histone DeacetylasesHumansMesenchymal Stem CellsMiceCore Binding Factor Alpha 1 SubunitCreb3 protein, mouseCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsFabp4 protein, mouseFatty Acid-Binding ProteinsHistone Deacetylase 3Histone DeacetylasesPPAR gammaRunx2 protein, mouse

Identifiers

PMID24948012
PMCPMC4158692
OpenAlexW1987966591

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.