Evidence map›Paper›PMID 26657771›Full record

ArticleDevelopment (Cambridge, England)2016

Dual function of Bmpr1a signaling in restricting preosteoblast proliferation and stimulating osteoblast activity in mouse.

Joohyun Lim, Yu Shi, Courtney M Karner, Seung-Yon Lee, Wen-Chih Lee, Guangxu He, Fanxin Long

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

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  5. CRISPR-mediated conditional mutagenesis ofbioRxiv : the preprint server for biology · 2026
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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

7 authors.

Joohyun LimDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA Division of Biology and Biomedical Sciences, Washington University School of Medicine, St Louis, MO 63110, USA.
Yu ShiDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA.
Courtney M KarnerDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA.
Seung-Yon LeeDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA.
Wen-Chih LeeDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA.
Guangxu HeDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA Department of Orthopedics, The Second Hospital of Xiangya, Central South University, Hunan 410013, People's Republic of China.
Fanxin LongDepartment of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO 63110, USA Division of Biology and Biomedical Sciences, Washington University School of Medicine, St Louis, MO 63110, USA Department of Medicine, Department of Developmental Biology, Washington University School of Medicine, St Louis, MO 63110, USA flong@wustl.edu.

Funding

The Role of the Osteoblast Secretome in Bone FormationP30AR057235 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2009 to 2018
$5.7M
Washington University Center for Kidney Disease ResearchP30DK079333 · NIDDK · WASHINGTON UNIVERSITY · PI HAMMERMAN, MARC RANDALL · 2007 to 2011
$5.1M
Mechanisms of WNT Signaling In BoneR01AR060456 · NIAMS · WASHINGTON UNIVERSITY · PI LONG, FANXIN · 2010 to 2020
$4.0M
Notch Signaling and Bone FormationR01AR055923 · NIAMS · WASHINGTON UNIVERSITY · PI LONG, FANXIN · 2008 to 2017
$3.5M
NIAMS NIH HHS AR055923NIAMS NIH HHS AR060456NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR055923NIAMS NIH HHS R01 AR060456NIDDK NIH HHS P30 DK079333
6 · The paper itself

Abstract

Exogenous bone morphogenetic proteins (Bmp) are well known to induce ectopic bone formation, but the physiological effect of Bmp signaling on normal bone is not completely understood. By deleting the receptor Bmpr1a in osteoblast lineage cells with Dmp1-Cre, we observed a dramatic increase in trabecular bone mass in postnatal mice, which was due to a marked increase in osteoblast number that was likely to be driven by hyperproliferation of Sp7(+) preosteoblasts. Similarly, inducible deletion of Bmpr1a in Sp7(+) cells specifically in postnatal mice increased trabecular bone mass. However, deletion of Smad4 by the same approaches had only a minor effect, indicating that Bmpr1a signaling suppresses trabecular bone formation through effectors beyond Smad4. Besides increasing osteoblast number in the trabecular bone, deletion of Bmpr1a by Dmp1-Cre also notably reduced osteoblast activity, resulting in attenuation of periosteal bone growth. The impairment in osteoblast activity correlated with reduced mTORC1 signaling in vivo, whereas inhibition of mTORC1 activity abolished the induction of protein anabolism genes by BMP2 treatment in vitro. Thus, physiological Bmpr1a signaling in bone exerts a dual function in both restricting preosteoblast proliferation and promoting osteoblast activity.

Indexed as

AnimalsBone Morphogenetic Protein Receptors, Type ICells, CulturedExtracellular Matrix ProteinsMiceOsteoblastsSignal TransductionBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type IDmp1 protein, mouseExtracellular Matrix ProteinsBmpBmpr1aMousemTORC1OsteoblastSmad4

Identifiers

PMID26657771
PMCPMC4725340

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.