Evidence map›Paper›PMID 29855498›Full record

ArticleScientific reports2018

BMPRIA is required for osteogenic differentiation and RANKL expression in adult bone marrow mesenchymal stromal cells.

Soma Biswas, Ping Li, Hongguang Wu, Md Shafiquzzaman, Shunichi Murakami, Michael D Schneider, Yuji Mishina, Baojie Li, Jing Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  7. [Latest Research Findings on the Regulation of Bone Homeostasis by ALK3].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022
    Review
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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

9 authors at 4 institutions in 4 countries.

Soma BiswasBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Ping LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Hongguang WuBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Md ShafiquzzamanBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China.
Shunichi MurakamiDepartment of Orthopaedics, Case Western Reserve University, Cleveland, Ohio, 44106, USA.
Michael D SchneiderBritish Heart Foundation Centre of Research Excellence, National Heart and Lung Institute, Imperial College London, London, W12 0NN, UK.ORCID 0000-0001-9645-1938
Yuji MishinaDepartment of Biologic & Materials Sciences, School of Dentistry, University of Michigan, 1011N, University Ave., Ann Arbor, MI, 48109, USA.
Baojie LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China. libj@sjtu.edu.cn.
Jing LiDepartment of Ophthalmology, XinHua Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China. lijing@xinhuamed.com.cn.ORCID 0000-0001-9250-7017
Shanghai Jiao Tong University · CNBritish Heart Foundation · GBCase Western Reserve University · USUniversity of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone morphogenetic proteins (BMPs) activate the canonical Smad1/5/8 and non-canonical Tak1-MAPK pathways via BMP receptors I and II to regulate skeletal development and bone remodeling. Specific ablation of Bmpr1a in immature osteoblasts, osteoblasts, or osteocytes results in an increase in cancellous bone mass, yet opposite results have been reported regarding the underlying mechanisms. Moreover, the role for BMPRIA-mediated signaling in bone marrow mesenchymal stromal cells (BM-MSCs) has not been explored. Here, we specifically ablated Bmpr1a in BM-MSCs in adult mice to study the function of BMPR1A in bone remodeling and found that the mutant mice showed an increase in cancellous and cortical bone mass, which was accompanied by a decrease in bone formation rate and a greater decrease in bone resorption. Decreased bone formation was associated with a defect in BM-MSC osteogenic differentiation whereas decreased bone resorption was associated with a decrease in RANKL production and osteoclastogenesis. However, ablation of Tak1, a critical non-canonical signaling molecule downstream of BMP receptors, in BM-MSCs at adult stage did not affect bone remodeling. These results suggest that BMP signaling through BMPRIA controls BM-MSC osteogenic differentiation/bone formation and RANKL expression/osteoclastogenesis in adult mice independent of Tak1 signaling.

Indexed as

Cell DifferentiationAnimalsBone and BonesBone Marrow CellsBone Morphogenetic Protein Receptors, Type IBone ResorptionCell LineageHomeodomain ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMesenchymal Stem CellsMiceMice, TransgenicOsteoblastsRANK LigandSignal TransductionBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type IHomeodomain ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesPrrx1 protein, mouseRANK LigandTnfsf11 protein, mouse

Identifiers

PMID29855498
PMCPMC5981611
OpenAlexW2806931643

What OpenQuestion holds

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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.