Evidence map›Paper›PMID 35386071›Full record

ArticleMolecular biology reports2022

Bmal1- and Per2-mediated regulation of the osteogenic differentiation and proliferation of mouse bone marrow mesenchymal stem cells by modulating the Wnt/β-catenin pathway.

Jiawen Zheng, Lanxin Zhang, Zhen Tan, Qing Zhao, Xiaoyu Wei, Yuqing Yang, Rong Li

Abstract read
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In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  16. Effect ofFrontiers in endocrinology · 2022
    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

7 authors at 1 institution in 1 country.

Jiawen Zheng *Orthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China.
Lanxin Zhang *Orthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China.
Zhen TanState Key Laboratory of Oral Diseases, Sichuan University, Chengdu, China. tzdentist@163.com.
Qing ZhaoOrthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China. fanfan_qing@163.com.
Xiaoyu WeiOrthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China.
Yuqing YangOrthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China.
Rong LiOrthodontic Centre, West China College of Stomatology, Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

the National Science Foundation of China 81371113the National Science Foundation of China 81870745
6 · The paper itself

Abstract

backgroundBmal1 and Per2 are the core components of the circadian clock genes (CCGs). Bmal1 METHODS AND

resultsLentiviral and adenoviral vectors were constructed to silence or overexpress Bmal1 or Per2 and MTT, flow cytometry, RT-qPCR, WB, immunohistochemistry, alizarin red staining and ChIP-Seq analyses were applied to identify the possible mechanism. The successful knockdown and overexpression of Bmal1/Per2 were detected by fluorescence microcopy. Flow cytometry found out that Bmal1 or Per2 knockdown resulted in G1-phase cell cycle arrest. RT-qPCR showed the different expression levels of Wnt-3a, c-myc1 and axin2 in the Wnt/β-catenin signaling pathway as well as the gene expression change of Rorα and Rev-erbα. Meanwhile, related proteins such as β-catenin, TCF-1, and P-GSK-3β were detected. ALP activity and the amount of mineral nodules were compared. ChIP-Seq results showed the possible mechanism.

conclusionsBmal1 and Per2, as primary canonical clock genes, showed synergistic effects on the proliferation and differentiation of BMSCs. They would inhibit the Wnt/β-catenin signaling pathway by downregulating Rorα expression or upregulating Rev-erbα expression, both of which were also key elements of CCGs. And this may be the mechanism by which they negatively regulate the osteogenic differentiation of BMSCs. Bmal1 and Per2 show synergistic effects in the proliferation of BMSCs. In addition, they play a synergistic role in negatively regulating the osteogenic differentiation ability of BMSCs. Bmal1 and Per2 may regulate the aging of BMSCs by altering cell proliferation and osteogenic differentiation through Rorα and Rev-erbα to affect Wnt/β-catenin pathway.

Indexed as

ARNTL Transcription Factorsbeta CateninOsteogenesisPeriod Circadian ProteinsWnt Signaling PathwayAnimalsBone Marrow CellsCell DifferentiationCell ProliferationCells, CulturedGlycogen Synthase Kinase 3 betaMiceARNTL Transcription Factorsbeta CateninBmal1 protein, mouseCTNNB1 protein, mouseGlycogen Synthase Kinase 3 betaPer2 protein, mousePeriod Circadian ProteinsAgingBMSCsCCGsOsteogenic differentiationProliferation

Identifiers

PMID35386071
OpenAlexW4226092282

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.