Evidence map›Paper›PMID 35414778›Full record

ArticleInternational journal of biological sciences2022

GPR125 positively regulates osteoclastogenesis potentially through AKT-NF-κB and MAPK signaling pathways.

Chen-Yi Tang, He Wang, Yan Zhang, Zhongliang Wang, Guochun Zhu, Abigail McVicar, Yi-Ping Li, Wei Chen

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Complex G-protein signaling of the adhesion GPCR, ADGRA3.The Journal of biological chemistry · 2025
    Article
  5. Article
  6. Review
  7. The function of GPCRs in different bone cells.International journal of biological sciences · 2025
    Review
  8. Article
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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

8 authors at 3 institutions in 2 countries.

Chen-Yi TangDepartment of Pathology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
He WangDepartment of Pathology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Yan ZhangDepartment of Pathology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Zhongliang WangEngineering Research Center of Molecular & Neuroimaging, Ministry of Education, School of Life Science and Technology, Xidian University, Xi'an, Shaanxi 710126, China.
Guochun ZhuDepartment of Pathology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Abigail McVicarDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, Louisiana, USA.
Yi-Ping LiDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, Louisiana, USA.
Wei ChenDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, Louisiana, USA.
University of Alabama at Birmingham · USTulane University · USXidian University · CN

Funding

Inhibiting Periodontitis by Targeting Cathepsin K and Attenuating TLR SignalingR01DE023813 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2014 to 2023
$3.9M
Mechanistic basis of the role of Cbx3 in negatively regulating osteoclast differentiation through epigenetic modificationR01AR075735 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2019 to 2024
$2.4M
Cbfβ mediates articular cartilage regeneration and repair in agingR01AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2019 to 2023
$2.1M
Gα13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitisR01DE028264 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2018 to 2022
$1.8M
Characterizing the negative signaling in dendritic cells and macrophages to attenuate inflammation and bone destruction in Rheumatoid arthritisR01AR074954 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2020 to 2024
$1.6M
Characterizing the mechanism by which endogenous negative regulators of osteoclasts control bone homeostasis under physiological and pathological conditions in mouse modelsR01AR070135 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2021
$1.6M
Cbfβ mediates articular cartilage regeneration and repair in agingR56AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2017
$371k
NIAMS NIH HHS R01 AR070135NIAMS NIH HHS R01 AR074954NIAMS NIH HHS R01 AR075735NIA NIH HHS R01 AG056438NIA NIH HHS R56 AG056438NIDCR NIH HHS R01 DE023813NIDCR NIH HHS R01 DE028264
6 · The paper itself

Abstract

G-protein-coupled receptors (GPCRs) signaling is critical to cell differentiation and activation. However, the function of GPCRs in osteoclast differentiation and activation remains unclear. We found that the G-protein coupled receptor 125 (GPCR 125) gene (Gpr125) gene was highly expressed in osteoclasts through RNA-sequencing technology, qRT-PCR, and Western blot analysis. We characterized the role of GPCR125 in osteoclast differentiation and activation by loss-of-function and gain-of-function methods in osteoclasts. Osteoclasts with lentivirus-mediated GPR125 silencing demonstrated a dramatic reduction in differentiation and impaired bone resorption function. In contrast, overexpression of Gpr125 in osteoclasts increased NFATC1 expression and enhanced osteoclast differentiation and enhanced osteoclast-mediated bone resorption. These results indicated that GPCR125 positively regulates osteoclast formation and function. Following receptor activator of nuclear factor kappa-Β ligand (RANKL) stimulation, the expression levels of MAPK signaling pathway proteins phosphorylated-ERK (p-ERK) and phosphorylated-p38 (p-p38) were significantly decreased in the Gpr125 knockdown (sh-GPR125) group compared to its control group. We also found that phosphorylated AKT (p-AKT) expression was downregulated, as well as nuclear factor kappa-B (NF-κB) signaling pathway protein phosphorylated-IKB alpha (p-IKBα). Our results demonstrated that GPCR125 positively regulates osteoclasts via RANKL-stimulated MAPK and AKT-NF-κB signaling pathways, and GPCR125 could potentially be utilized as a novel therapeutic target in bone related diseases including osteoporosis.

Indexed as

Bone ResorptionOsteogenesisAnimalsCell DifferentiationMiceNF-kappa BOsteoclastsProto-Oncogene Proteins c-aktRANK LigandReceptors, G-Protein-CoupledSignal TransductionNF-kappa BProto-Oncogene Proteins c-aktRANK LigandReceptors, G-Protein-CoupledAkt signaling pathwaybone resorptionGPCR 125Gpr125MAPK signaling pathwayNFκB signaling pathwayosteoclasts

Identifiers

PMID35414778
PMCPMC8990458
OpenAlexW4226425304

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.