Evidence map›Paper›PMID 28377961›Full record

ArticleBone reports2015

Osteoporotic bone of miR-150-deficient mice: Possibly due to low serum OPG-mediated osteoclast activation.

Sik-Won Choi, Su Ui Lee, Eun Hye Kim, Sang-Joon Park, Inpyo Choi, Tae-Don Kim, Seong Hwan Kim

Open access · goldAbstract read
In one paragraph

Article in Bone reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Extracellular vesicle-mediated crosstalk in bone: miR-150-5p as a mechanosensitive regulator of osteoclastogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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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 4 institutions in 1 country.

Sik-Won ChoiLaboratory of Translational Therapeutics, Korea Research Institute of Chemical Technology, Daejeon 305-600, Republic of Korea.
Su Ui LeeNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju-si, Chungbuk 363-883, Republic of Korea.
Eun Hye KimLaboratory of Translational Therapeutics, Korea Research Institute of Chemical Technology, Daejeon 305-600, Republic of Korea.
Sang-Joon ParkDepartment of Histology, College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea.
Inpyo ChoiImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea; Department of Functional Genomics, Korea University of Science and Technology, Daejeon 305-333, Republic of Korea.
Tae-Don KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea; Department of Functional Genomics, Korea University of Science and Technology, Daejeon 305-333, Republic of Korea.
Seong Hwan KimLaboratory of Translational Therapeutics, Korea Research Institute of Chemical Technology, Daejeon 305-600, Republic of Korea.
Korea Research Institute of Chemical Technology · KRKorea University of Science and Technology · KRKorea Research Institute of Bioscience and Biotechnology · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miR)-150 has been shown to control B and T cell differentiation in the bone marrow. The regulation of B and T cells is directly or systematically associated with bone remodeling cells such as osteoclasts; however, the functional role of miR-150 in bone homeostasis has not been well studied. Here, we observed down-regulation of miR-150 during in vitro osteoclast differentiation and, furthermore, that miR-150 knockout mice exhibit decreased bone mass and an increased number of osteoclasts. miR-150 deficiency did not affect osteoclast differentiation, but miR150 knockout mice had significantly lower osteoprotegrin (OPG) serum levels, suggesting that the reduction of serum OPG level in miR-150 knockout mice might induce B cell expansion and subsequently increase serum levels of immunoglobulins for activating osteoclast differentiation.

Indexed as

BMC, bone marrow cellBMD, bone mineral densityBMMs, bone marrow-derived macrophagesBoneBV/TV, bone volume/tissue volumeIFN, interferonIg, immunoglobuliniNKT, invariant NK T cellM-CSF, macrophage-colony-stimulating factormiR-150miRNA, microRNAMNCs, multinucleated osteoclast cellsNK, natural killerOPG, osteoprotegrinOsteoclastsOsteoporosisOsteoprotegrinRANKL, receptor activator of nuclear factor-kB ligandTb.N, number of trabeculaeTb.Sp, trabecular separationTNF, tumor necrosis factorTRAP, tartrate-resistant acid phosphatase

Identifiers

PMID28377961
PMCPMC5365209
OpenAlexW813289493

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.