Evidence map›Paper›PMID 20571024›Full record

ArticleThe Journal of biological chemistry2010

Deficiency of chemokine receptor CCR1 causes osteopenia due to impaired functions of osteoclasts and osteoblasts.

Akiyoshi Hoshino, Tadahiro Iimura, Satoshi Ueha, Sanshiro Hanada, Yutaka Maruoka, Mitsuori Mayahara, Keiko Suzuki, Toshio Imai, Masako Ito, Yoshinobu Manome and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  12. Osteoclasts Derive Predominantly from Bone Marrow-Resident CXJournal of immunology (Baltimore, Md. : 1950) · 2020
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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

15 authors at 7 institutions in 1 country.

Akiyoshi HoshinoInternational Clinical Research Center, Research Institute, International Medical Center of Japan, Tokyo 162-8655, Japan.
Tadahiro Iimura
Satoshi Ueha
Sanshiro Hanada
Yutaka Maruoka
Mitsuori Mayahara
Keiko Suzuki
Toshio Imai
Masako Ito
Yoshinobu Manome
Masato Yasuhara
Takaaki Kirino
Akira Yamaguchi
Kouji Matsushima
Kenji Yamamoto
Saitama International Medical Center · JPTokyo Medical and Dental University · JPJikei University School of Medicine · JPShowa University · JPKAN Research Institute · JPTokyo Medical and Dental University Hospital · JPUniversity of Nagasaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines are characterized by the homing activity of leukocytes to targeted inflammation sites. Recent research indicates that chemokines play more divergent roles in various phases of pathogenesis as well as immune reactions. The chemokine receptor, CCR1, and its ligands are thought to be involved in inflammatory bone destruction, but their physiological roles in the bone metabolism in vivo have not yet been elucidated. In the present study, we investigated the roles of CCR1 in bone metabolism using CCR1-deficient mice. Ccr1(-/-) mice have fewer and thinner trabecular bones and low mineral bone density in cancellous bones. The lack of CCR1 affects the differentiation and function of osteoblasts. Runx2, Atf4, Osteopontin, and Osteonectin were significantly up-regulated in Ccr1(-/-) mice despite sustained expression of Osterix and reduced expression of Osteocalcin, suggesting a lower potential for differentiation into mature osteoblasts. In addition, mineralized nodule formation was markedly disrupted in cultured osteoblastic cells isolated from Ccr1(-/-) mice. Osteoclastogenesis induced from cultured Ccr1(-/-) bone marrow cells yielded fewer and smaller osteoclasts due to the abrogated cell-fusion. Ccr1(-/-) osteoclasts exerted no osteolytic activity concomitant with reduced expressions of Rank and its downstream targets, implying that the defective osteoclastogenesis is involved in the bone phenotype in Ccr1(-/-) mice. The co-culture of wild-type osteoclast precursors with Ccr1(-/-) osteoblasts failed to facilitate osteoclastogenesis. This finding is most likely due to a reduction in Rankl expression. These observations suggest that the axis of CCR1 and its ligands are likely to be involved in cross-talk between osteoclasts and osteoblasts by modulating the RANK-RANKL-mediated interaction.

Indexed as

Cell CommunicationAnimalsAntigens, DifferentiationBone DensityBone Marrow CellsBone ResorptionCell DifferentiationCells, CulturedChemokinesCoculture TechniquesFemaleGene Expression RegulationMaleMiceMice, KnockoutOsteoblastsAntigens, DifferentiationCcr1 protein, mouseChemokinesReceptors, CCR1

Identifiers

PMID20571024
PMCPMC2937910
OpenAlexW2110450018

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.