Evidence map›Paper›PMID 32790690›Full record

ArticlePloS one2020

Knockdown of Tcirg1 inhibits large-osteoclast generation by down-regulating NFATc1 and IP3R2 expression.

Dongyan Zhang, Liying Lin, Bingwu Yang, Zhen Meng, Bin Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Dongyan ZhangDepartment of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Shandong University & Shandong Provincial Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan, Shandong, PR China.
Liying LinDepartment of Stomatology & Key Laboratory of Oral Maxillofacial-Head and Neck Medical Biology of Shandong Province & Precision Biomedical Key Laboratory, Liaocheng People's Hospital, Liaocheng, Shandong, PR China.
Bingwu YangDepartment of Stomatology & Key Laboratory of Oral Maxillofacial-Head and Neck Medical Biology of Shandong Province & Precision Biomedical Key Laboratory, Liaocheng People's Hospital, Liaocheng, Shandong, PR China.
Zhen MengDepartment of Stomatology & Key Laboratory of Oral Maxillofacial-Head and Neck Medical Biology of Shandong Province & Precision Biomedical Key Laboratory, Liaocheng People's Hospital, Liaocheng, Shandong, PR China.
Bin ZhangDepartment of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Shandong University & Shandong Provincial Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan, Shandong, PR China.ORCID 0000-0002-5067-8544
Liaocheng People's Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TCIRG1 gene encodes the a3 isoform of vacuolar H+-ATPase (V-ATPase), which forms a proton transport channel in osteoclasts. Defects in this gene lead to functional impairment of osteoclasts and increased bone mass; however, the molecular mechanisms of TCIRG1 loss have not been fully elucidated. In the current study, we transfected mouse bone marrow-derived monocytes with control or Tcirg1-knockdown lentiviruses to further investigate the mechanisms of TCIRG1. Our results demonstrate that knockdown of Tcirg1 inhibits large-osteoclast (>100 μm) generation by decreasing the expression of nuclear factor of activated T-cells 1 (NFATc1) and inositol-1,4,5-trisphosphate receptor 2 (IP3R2). The decreased IP3R2 reduces intracellular calcium levels, which limits the nuclear translocation of NFATc1 in RANKL-induced mouse bone marrow-derived monocytes. These findings provide a mechanism to explain the effects of TCIRG1 impairment, with potential implications for the development of therapies for osteopetrosis.

Indexed as

Down-RegulationOsteogenesisAnimalsCells, CulturedGene Knockdown TechniquesInositol 1,4,5-Trisphosphate ReceptorsMaleMiceNFATC Transcription FactorsOsteoclastsVacuolar Proton-Translocating ATPasesAtp6ap1 protein, mouseInositol 1,4,5-Trisphosphate ReceptorsIp3r2 protein, mouseNfatc1 protein, mouseNFATC Transcription FactorsVacuolar Proton-Translocating ATPases

Identifiers

PMID32790690
PMCPMC7425954
OpenAlexW3049257988

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.