Evidence map›Paper›PMID 25909889›Full record

ArticleCell death and differentiation2015

Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

X Yuan, J Cao, T Liu, Y-P Li, F Scannapieco, X He, M J Oursler, X Zhang, J Vacher, C Li and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. 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
2.6field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

  1. Review
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  16. Regulator of G Protein Signaling Protein 12 (Rgs12) Controls Mouse Osteoblast Differentiation via Calcium Channel/Oscillation and Gαi-ERK Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  17. Review
  18. Article
  19. [Progress in the regulation of bone remodeling at the cellular level].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2017
    Review
  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

12 authors at 1 institution in 1 country.

X YuanDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
J CaoUSDA Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202, USA.
T LiuDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
Y-P LiDepartment of Pathology, University of Alabama at Birmingham (UAB), Birmingham, AL 35294, USA.
F ScannapiecoDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
X HeDepartment of Stomatology, The Fourth Affiliated Hospital of China Medical University, China Medical University, Shenyang, Liaoning 110032, China.
M J OurslerDepartment of Medicine, Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA.
X ZhangDepartment of Orthopedics, Center for Musculoskeletal Research, University of Rochester Medical Center, School of Medicine and Dentistry, Rochester, NY 14642, USA.
J VacherDepartment of Medicine, Division of Experimental Medicine, The Institut de Recherches Cliniques de Montréal, University of Montreal, Montreal, Quebec H2W 1R7, Canada.
C LiDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
D OlsonDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
S YangDepartment of Oral Biology, University at Buffalo, School of Dental Medicine, The State University of New York, Buffalo, NY 14214, USA.
University at Buffalo, State University of New York · US

Funding

Regulation of skeletal development and homeostasis by IFT proteinR01DE023105 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$2.0M
Role of RGS12, a Regulator of G protein Signaling, in Bone RemodelingR01AR066101 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.8M
Function of Regulator of G protein signaling in aging skeletonR01AG048388 · NIA · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.7M
The role of IFT80 in bone formationR03AR061052 · NIAMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YANG, SHUYING · 2012 to 2014
$232k
NIAMS NIH HHS AR061052NIAMS NIH HHS AR066101NIAMS NIH HHS R01 AR066101NIAMS NIH HHS R03 AR061052NIA NIH HHS AG048388NIA NIH HHS R01 AG048388NIDCR NIH HHS R01 DE023105
6 · The paper itself

Abstract

Regulators of G protein signaling (Rgs) have pivotal roles in controlling various cellular processes, such as cell differentiation. How Rgs proteins regulate osteoclast (OC) differentiation, function and bone homeostasis is poorly understood. It was previously demonstrated that Rgs12, the largest protein in the Rgs family, is predominantly expressed in OCs and regulates OC differentiation in vitro. To further understand the role and mechanism of Rgs12 in OC differentiation and bone diseases in vivo, we created OC-targeted Rgs12 knockout mice by using inducible Mx1-Cre and CD11b-Cre. Deletion of Rgs12 in hematopoietic cells or specifically in OC precursors resulted in increased bone mass with decreased OC numbers. Loss of Rgs12 impaired OC differentiation and function with impaired Ca(2+) oscillations and reduced nuclear factor of activated T cells (NFAT) 2 expression. The introduction of wild-type osteoblasts did not rescue the defective osteoclastogenesis. Ectopic expression of NFAT2 rescued defective OC differentiation in CD11b;Rgs12(fl/fl) cells and promoted normal OC differentiation. Moreover, deletion of Rgs12 significantly inhibited pathological osteoclastogenesis and bone destruction in Rgs12-deficient mice that were subjected to ovariectomy and lipodysaccharide for bone loss. Thus our findings demonstrate that Rgs12 is an important regulator in OC differentiation and function and identify Rgs12 as a potential therapeutic target for osteoporosis and inflammation-induced bone loss.

Indexed as

Bone RemodelingAnimalsBone and BonesBone Marrow CellsCalciumCD11b AntigenCell DifferentiationCells, CulturedFemurHematopoietic Stem CellsLipopolysaccharidesMiceMice, KnockoutMice, TransgenicNFATC Transcription FactorsOsteoclastsCalciumCD11b AntigenLipopolysaccharidesNfatc1 protein, mouseNFATC Transcription FactorsRGS12 protein, mouseRGS Proteins

Identifiers

PMID25909889
PMCPMC4816106
OpenAlexW2020597676

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.