Evidence map›Paper›PMID 26344756›Full record

ArticleBone2015

Bmp2 conditional knockout in osteoblasts and endothelial cells does not impair bone formation after injury or mechanical loading in adult mice.

Sarah Howe McBride-Gagyi, Jennifer A McKenzie, Evan G Buettmann, Michael J Gardner, Matthew J Silva

Abstract read
In one paragraph

Article in Bone, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  9. Bone phenotyping of murine hemochromatosis models with deficiencies of Hjv, Alk2, or Alk3: The influence of sex and the bone compartment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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 1 institution in 1 country.

Sarah Howe McBride-GagyiDepartment of Orthopaedic Surgery, Saint Louis University School of Medicine, 1402 S. Grand Blvd, Schwitalla Hall, M176, St. Louis, MO 63104, USA; Department of Orthopedic Surgery, Washington University in St. Louis School of Medicine, 660 S. Euclid, Campus Box8233, St. Louis, MO 63110, USA. Electronic address: SMcBrid9@slu.edu.
Jennifer A McKenzieDepartment of Orthopedic Surgery, Washington University in St. Louis School of Medicine, 660 S. Euclid, Campus Box8233, St. Louis, MO 63110, USA. Electronic address: McKenzieJ@wudosis.wustl.edu.
Evan G BuettmannDepartment of Orthopedic Surgery, Washington University in St. Louis School of Medicine, 660 S. Euclid, Campus Box8233, St. Louis, MO 63110, USA. Electronic address: BuettmannE@wustl.edu.
Michael J GardnerDepartment of Orthopedic Surgery, Washington University in St. Louis School of Medicine, 660 S. Euclid, Campus Box8233, St. Louis, MO 63110, USA. Electronic address: GardnerM@wudosis.wustl.edu.
Matthew J SilvaDepartment of Orthopedic Surgery, Washington University in St. Louis School of Medicine, 660 S. Euclid, Campus Box8233, St. Louis, MO 63110, USA. Electronic address: SilvaM@wudosis.wustl.edu.
Washington University in St. Louis · US

Funding

Washington University Center for Translational NeuroscienceP30NS057105 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2006 to 2011
$8.7M
The Role of the Osteoblast Secretome in Bone FormationP30AR057235 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2009 to 2018
$5.7M
OSTEOGENIC AND ANGIOGENIC RESPONSE TO SKELETAL LOADINGR01AR050211 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2003 to 2020
$5.0M
Skeletal Disorders Training ProgramT32AR060719 · NIAMS · WASHINGTON UNIVERSITY · PI Roberto Civitelli · 2011 to 2026
$4.6M
INTERDISCIPLINARY TRAINING IN MECHANOBIOLOGY FROM NM TO CMT32EB018266 · NIBIB · WASHINGTON UNIVERSITY · PI BAYLY, PHILIP V · 2014 to 2018
$987k
IN VIVO MICROCT SYSTEMS10RR023660 · NCRR · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J. · 2007 to 2007
$317k
NCRR NIH HHS S10 RR023660NIAMS NIH HHS 1T32AR060719-01NIAMS NIH HHS AR050211NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR050211NIAMS NIH HHS T32 AR060719NIBIB NIH HHS T32 EB018266NINDS NIH HHS P30 NS057105
6 · The paper itself

Abstract

Post-natal osteogenesis after mechanical trauma or stimulus occurs through either endochondral healing, intramembranous healing or lamellar bone formation. Bone morphogenetic protein 2 (BMP2) is up-regulated in each of these osteogenic processes and is expressed by a variety of cells including osteoblasts and vascular cells. It is known that genetic knockout of Bmp2 in all cells or in osteo-chondroprogenitor cells completely abrogates endochondral healing after full fracture. However, the importance of BMP2 from differentiated osteoblasts and endothelial cells is not known. Moreover, the importance of BMP2 in non-endochondral bone formation such as intramembranous healing or lamellar bone formation is not known. Using inducible and tissue-specific Cre-lox mediated targeting of Bmp2 in adult (10-24 week old) mice, we assessed the role of BMP2 expression globally, by osteoblasts, and by vascular endothelial cells in endochondral healing, intramembranous healing and lamellar bone formation. These three osteogenic processes were modeled using full femur fracture, ulnar stress fracture, and ulnar non-damaging cyclic loading, respectively. Our results confirmed the requirement of BMP2 for endochondral fracture healing, as mice in which Bmp2 was knocked out in all cells prior to fracture failed to form a callus. Targeted deletion of Bmp2 in osteoblasts (osterix-expressing) or vascular endothelial cells (vascular endothelial cadherin-expressing) did not impact fracture healing in any way. Regarding non-endochondral bone formation, we found that BMP2 is largely dispensable for intramembranous bone formation after stress fracture and also not required for lamellar bone formation induced by mechanical loading. Taken together our results indicate that osteoblasts and endothelial cells are not a critical source of BMP2 in endochondral fracture healing, and that non-endochondral bone formation in the adult mouse is not as critically dependent on BMP2.

Indexed as

AnimalsBone Morphogenetic Protein 2Endothelial CellsFemaleFracture HealingFractures, StressGene ExpressionMaleMiceMice, KnockoutOsteoblastsOsteogenesisStress, MechanicalBmp2 protein, mouseBone Morphogenetic Protein 2BMP2Bone homeostasisBone injuryFacture healingOrthopedicsOsteoblasts

Identifiers

PMID26344756
PMCPMC4640950
OpenAlexW1257409488

What OpenQuestion holds

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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.