Evidence map›Paper›PMID 29138422›Full record

ArticleScientific reports2017

FAM19A5, a brain-specific chemokine, inhibits RANKL-induced osteoclast formation through formyl peptide receptor 2.

Min Young Park, Hyung Sik Kim, Mingyu Lee, Byunghyun Park, Ha Young Lee, Eun Bee Cho, Jae Young Seong, Yoe-Sik Bae

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  6. Can Adipokine FAM19A5 Be a Biomarker of Metabolic Disorders?Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  7. Formyl peptide receptors in bone research.Connective tissue research · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. FAM19A1, a brain-enriched and metabolically responsive neurokine, regulates food intake patterns and mouse behaviors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Article
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

8 authors at 2 institutions in 1 country.

Min Young ParkDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
Hyung Sik KimDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
Mingyu LeeDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Byunghyun ParkDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
Ha Young LeeDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
Eun Bee ChoGraduate School of Medicine, Korea University, Seoul, Republic of Korea.
Jae Young SeongGraduate School of Medicine, Korea University, Seoul, Republic of Korea.
Yoe-Sik BaeDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea. yoesik@skku.edu.
Sungkyunkwan University · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoclasts can be differentiated from bone marrow-derived macrophages (BMDM). They play a key role in bone resorption. Identifying novel molecules that can regulate osteoclastogenesis has been an important issue. In this study, we found that FAM19A5, a neurokine or brain-specific chemokine, strongly stimulated mouse BMDM, resulting in chemotactic migration and inhibition of RANKL-induced osteoclastogenesis. Expression levels of osteoclast-related genes such as RANK, TRAF6, OSCAR, TRAP, Blimp1, c-fos, and NFATc1 were markedly decreased by FAM19A5. However, negative regulators of osteoclastogenesis such as MafB and IRF-8 were upregulated by FAM19A5. FAM19A5 also downregulated expression levels of RANKL-induced fusogenic genes such as OC-STAMP, DC-STAMP, and Atp6v0d2. FAM19A5-induced inhibitory effect on osteoclastogenesis was significantly reversed by a formyl peptide receptor (FPR) 2 antagonist WRW4 or by FPR2-deficiency, suggesting a crucial role of FPR2 in the regulation of osteoclastogenesis. Collectively, our results suggest that FAM19A5 and its target receptor FPR2 can act as novel endogenous ligand/receptor to negatively regulate osteoclastogenesis. They might be regarded as potential targets to control osteoclast formation and bone disorders.

Indexed as

AnimalsBone ResorptionBrainCell DifferentiationChemokinesCytokinesGene Expression Regulation, DevelopmentalHumansMacrophagesMiceOligopeptidesOsteoclastsOsteogenesisRANK LigandReceptors, Formyl PeptideChemokinesCytokinesformyl peptide receptor 2, mouseOligopeptidesRANK LigandReceptors, Formyl PeptideTafa5 protein, mouseTnfsf11 protein, mousetryptophyl-arginyl-tryptophyl-tryptophyl-tryptophyl-tryptophanamide

Identifiers

PMID29138422
PMCPMC5686125
OpenAlexW2767578613

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.