Evidence map›Paper›PMID 29691366›Full record

ArticleCell death & disease2018

Mutual inhibition between HDAC9 and miR-17 regulates osteogenesis of human periodontal ligament stem cells in inflammatory conditions.

Liya Li, Wenjia Liu, Hong Wang, Qianjuan Yang, Liqiang Zhang, Fang Jin, Yan Jin

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 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

7 authors at 1 institution in 1 country.

Liya LiState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Disease, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.
Wenjia LiuState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Disease, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.
Hong WangState Key Laboratory of Military Stomatology, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.
Qianjuan YangState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Disease, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.
Liqiang ZhangState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Disease, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.
Fang JinState Key Laboratory of Military Stomatology, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China. fangjin@fmmu.edu.cn.
Yan JinState Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Disease, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, 710032, Xi'an, Shaanxi, China. yanjin@fmmu.edu.cn.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylases (HDAC) plays important roles in the post-translational modifications of histone cores as well as non-histone targets. Many of them are involved in key inflammatory processes. Despite their importance, whether and how HDAC9 is regulated under inflammatory conditions remains unclear. The aim of this study was to evaluate the effects of HDAC9 under chronic inflammation condition in human periodontal ligament stromal cell (PDLSCs) and to explore the underlying regulatory mechanism. PDLSCs from healthy or periodontitis human tissue was compared. The therapeutic effects of HDAC inhibitors was determined in PDLSC pellet transplanted nude mice and LPS-induced rat periodontitis. We report that HDAC9 was the most affected HDAC family member under inflammatory conditions in PDLSCs. HDAC9 impaired osteogenic differentiation capacity of PDLSCs under inflammatory conditions. Downregulation of HDAC9 by HDAC inhibitors or si-HDAC9 rescued the osteogenic differentiation capacity of inflammatory PDLSC to a similar level with the healthy PDLSC. In this context, HDAC9 and miR-17 formed an inhibitory loop. The inhibition of miR-17 aggravated loss of calcified nodules in inflamed PDLSCs and interrupted the effect of HDAC inhibitor in rescuing osteogenesis. In vivo experiments using nude mice and LPS-induced periodontitis model confirmed that HDAC inhibitors could improve new bone formation. We conclude that HDAC inhibitors improved osteogenesis of PDLSCs in vitro and periodontitis in vivo.

Indexed as

Cell DifferentiationOsteogenesisAdolescentAdultAnimalsDisease Models, AnimalFemaleHistone Deacetylase InhibitorsHistone DeacetylasesHumansMaleMice, NudeMicroRNAsMiddle AgedPeriodontal LigamentPeriodontitisHDAC9 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesMicroRNAsMIRN17 microRNA, humanRepressor Proteins

Identifiers

PMID29691366
PMCPMC5915523
OpenAlexW2802780549

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.