Evidence map›Paper›PMID 30030453›Full record

ArticleScientific reports2018

Evidence for excessive osteoclast activation in SIRT6 null mice.

Demao Zhang, Junjun Jing, Feng Lou, Ruimin Li, Yilin Ping, Fanyuan Yu, Fanzi Wu, Xiao Yang, Ruoshi Xu, Feifei Li and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 29 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

17 authors at 3 institutions in 1 country.

Demao ZhangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Junjun JingState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Feng LouState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Ruimin LiDepartment of Endodontics, Stomatology Hospital, General Hospital of NingXia Medical University, Yinchuan, China.
Yilin PingDepartment of Stomatology, Tongde Hospital of Zhejiang Province, Zhejiang, China.
Fanyuan YuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Fanzi WuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Xiao YangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Ruoshi XuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Feifei LiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Ke WangDepartment of Biomedical Sciences, Texas A&M College of Dentistry, Dallas, TX, USA.
Mingru BaiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Caixia PiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jing XieState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. xiejing2012@scu.edu.cn.ORCID 0000-0001-8156-0322
Liwei ZhengState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Ling YeState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Xuedong ZhouState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. zhouxd@scu.edu.cn.
Sichuan University · CNNingxia Medical University · CNTongde Hospital of Zhejiang Province · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81371136National Natural Science Foundation of China (National Science Foundation of China) 81430011National Natural Science Foundation of China (National Science Foundation of China) 81600840National Natural Science Foundation of China (National Science Foundation of China) 81771047
6 · The paper itself

Abstract

SIRT6 is a NAD-dependent histone 3 deacetylase. SIRT6 null mice have been reported suffering osteopenia. However, the role of SIRT6 in bone resorption is still not well understood. In this study, we focused on the role of SIRT6 in osteoclast. We performed histological analysis on the femur, spine, alveolar bone and even tail of mutant mice, and found the bone mass is sharply decreased while the osteoclast activity is significantly increased. These phenotypes were further demonstrated by the osteoclast differentiation in cell-cultures with TRAP staining and Pit Resorption Assay. We next found the proliferation activity of mutant osteoclast precursors was increased, which might account for the enhanced osteoclast formation. The concentration of tartrate-resistant acid phosphatase 5b, a marker of osteoclast differentiation, was significantly higher in the mutant mice than control. Besides, the osteoclastogenic and NF-κB signaling related genes were significantly up-regulated. Moreover, osteoblast/osteoclast co-culture demonstrated that SIRT6 regulated osteoclast mainly through osteoblast paracrine manner, rather than osteoclast-autonomous behavior. Together, the enhanced osteoclast activation in SIRT6 null mice might be regulated by the hyperactive NF-κB signaling and the enhanced proliferation activity of osteoclast precursors through osteoblast paracrine manner at the cellular level.

Indexed as

AnimalsBone ResorptionCell DifferentiationCell ProliferationCells, CulturedMiceNF-kappa BOsteoblastsOsteoclastsParacrine CommunicationSignal TransductionSirtuinsTartrate-Resistant Acid PhosphataseNF-kappa BSirt6 protein, mouseSirtuinsTartrate-Resistant Acid Phosphatase

Identifiers

PMID30030453
PMCPMC6054613
OpenAlexW2884481535

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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.