Evidence map›Paper›PMID 27901049›Full record

ArticleScientific reports2016

Glucocorticoid receptor and Histone deacetylase 6 mediate the differential effect of dexamethasone during osteogenesis of mesenchymal stromal cells (MSCs).

Marilyn G Rimando, Hao-Hsiang Wu, Yu-An Liu, Chien-Wei Lee, Shu-Wen Kuo, Yin-Ping Lo, Kuo-Fung Tseng, Yi-Shiuan Liu, Oscar Kuang-Sheng Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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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

9 authors at 5 institutions in 1 country.

Marilyn G RimandoMolecular Medicine Program, Taiwan International Graduate Program, Academia Sinica and Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
Hao-Hsiang WuInstitute of Biophotonics, National Yang-Ming University, Taipei 11221, Taiwan.
Yu-An LiuInstitute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Chien-Wei LeeProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan.
Shu-Wen KuoInstitute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Yin-Ping LoProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan.
Kuo-Fung TsengDepartment of Orthopaedics, Cheng-Hsin General Hospital, Taipei 11220, Taiwan.
Yi-Shiuan LiuInstitute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Oscar Kuang-Sheng LeeInstitute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
National Yang Ming Chiao Tung University · TWAcademia Sinica · TWCheng Hsin General Hospital · TWInstitute of Molecular Biology, Academia Sinica · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lineage commitment and differentiation of mesenchymal stromal cells (MSCs) into osteoblasts in vitro is enhanced by a potent synthetic form of glucocorticoid (GC), dexamethasone (Dex). Paradoxically, when used chronically in patients, GCs exert negative effects on bone, a phenomenon known as glucocorticoid-induced osteoporosis in clinical practice. The mechanism on how GC differentially affects bone precursor cells to become mature osteoblasts during osteogenesis remains elusive. In this study, the dose and temporal regulation of Dex on MSC differentiation into osteoblasts were investigated. We found that continuous Dex treatment led to a net reduction of the maturation potential of differentiating osteoblasts. This phenomenon correlated with a decrease in glucocorticoid receptor (GR) expression, hastened degradation, and impaired sub cellular localization. Similarly, Histone Deacetylase 6 (HDAC6) expression was found to be regulated by Dex, co-localized with GR and this GR-HDAC6 complex occupied the promoter region of the osteoblast late marker osteocalcin (OCN). Combinatorial inhibition of HDAC6 and GR enhanced OCN expression. Together, the cross-talk between the Dex effector molecule GR and the inhibitory molecule HDAC6 provided mechanistic explanation of the bimodal effect of Dex during osteogenic differentiation of MSCs. These findings may provide new directions of research to combat glucocorticoid-induced osteoporosis.

Indexed as

Alkaline PhosphataseAnimalsCell DifferentiationCell LineCell Line, TumorCells, CulturedDexamethasoneGene ExpressionGlucocorticoidsHistone Deacetylase 6HumansMesenchymal Stem CellsMice, Inbred BALB COsteoblastsOsteogenesisReceptors, GlucocorticoidAlkaline PhosphataseDexamethasoneGlucocorticoidsHistone Deacetylase 6Receptors, Glucocorticoid

Identifiers

PMID27901049
PMCPMC5128810
OpenAlexW2557347661

What OpenQuestion holds

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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.