Evidence map›Paper›PMID 27102547›Full record

ArticleBone2016

Sostdc1 deficiency accelerates fracture healing by promoting the expansion of periosteal mesenchymal stem cells.

Nicole M Collette, Cristal S Yee, Nicholas R Hum, Deepa K Murugesh, Blaine A Christiansen, LiQin Xie, Aris N Economides, Jennifer O Manilay, Alexander G Robling, Gabriela G Loots

Open access · hybridAbstract read
In one paragraph

Article in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  6. Sostdc1 Suppression in the Absence of Sclerostin Potentiates Anabolic Action of Cortical Bone in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  7. Review
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  15. Article
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  17. Niches for Skeletal Stem Cells of Mesenchymal Origin.Frontiers in cell and developmental biology · 2020
    Review
  18. Article
  19. 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

10 authors at 5 institutions in 1 country.

Nicole M ColletteBiology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA.
Cristal S YeeBiology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA; Molecular and Cell Biology Unit, School of Natural Sciences, University of California at Merced, Merced, CA, USA.
Nicholas R HumBiology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA.
Deepa K MurugeshBiology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA.
Blaine A ChristiansenUniversity of California Davis Medical Center, Sacramento, CA, USA.
LiQin XieRegeneron Pharmaceuticals, Tarrytown, NY, USA.
Aris N EconomidesRegeneron Pharmaceuticals, Tarrytown, NY, USA.
Jennifer O ManilayMolecular and Cell Biology Unit, School of Natural Sciences, University of California at Merced, Merced, CA, USA.
Alexander G RoblingIndiana University, Indianapolis, IN, USA.
Gabriela G LootsBiology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA; Molecular and Cell Biology Unit, School of Natural Sciences, University of California at Merced, Merced, CA, USA. Electronic address: loots1@llnl.gov.
Lawrence Livermore National Laboratory · USRegeneron (United States) · USIndiana University – Purdue University Indianapolis · USUniversity of California Davis Medical Center · USUniversity of California, Merced · US

Funding

MECHANISMS OF INHIBITING BONE FORMATION THROUGH ANTAGONISMR01DK075730 · NIDDK · UNIVERSITY OF CALIF-LAWRNC LVRMR NAT LAB · PI LOOTS, GABRIELA G · 2009 to 2013
$1.8M
NIDDK NIH HHS R01 DK075730
6 · The paper itself

Abstract

Loss of Sostdc1, a growth factor paralogous to Sost, causes the formation of ectopic incisors, fused molars, abnormal hair follicles, and resistance to kidney disease. Sostdc1 is expressed in the periosteum, a source of osteoblasts, fibroblasts and mesenchymal progenitor cells, which are critically important for fracture repair. Here, we investigated the role of Sostdc1 in bone metabolism and fracture repair. Mice lacking Sostdc1 (Sostdc1(-/-)) had a low bone mass phenotype associated with loss of trabecular bone in both lumbar vertebrae and in the appendicular skeleton. In contrast, Sostdc1(-/-) cortical bone measurements revealed larger bones with higher BMD, suggesting that Sostdc1 exerts differential effects on cortical and trabecular bone. Mid-diaphyseal femoral fractures induced in Sostdc1(-/-) mice showed that the periosteal population normally positive for Sostdc1 rapidly expands during periosteal thickening and these cells migrate into the fracture callus at 3days post fracture. Quantitative analysis of mesenchymal stem cell (MSC) and osteoblast populations determined that MSCs express Sostdc1, and that Sostdc1(-/-) 5day calluses harbor >2-fold more MSCs than fractured wildtype controls. Histologically a fraction of Sostdc1-positive cells also expressed nestin and α-smooth muscle actin, suggesting that Sostdc1 marks a population of osteochondral progenitor cells that actively participate in callus formation and bone repair. Elevated numbers of MSCs in D5 calluses resulted in a larger, more vascularized cartilage callus at day 7, and a more rapid turnover of cartilage with significantly more remodeled bone and a thicker cortical shell at 21days post fracture. These data support accelerated or enhanced bone formation/remodeling of the callus in Sostdc1(-/-) mice, suggesting that Sostdc1 may promote and maintain mesenchymal stem cell quiescence in the periosteum.

Indexed as

Fracture HealingActinsAdaptor Proteins, Signal TransducingAnimalsBiomechanical PhenomenaBone Morphogenetic ProteinsBony CallusCalcification, PhysiologicCancellous BoneCell DifferentiationCell ProliferationCortical BoneFemurGene DeletionMesenchymal Stem CellsMice, Inbred C57BLActinsAdaptor Proteins, Signal Transducingalpha-smooth muscle actin, mouseBone Morphogenetic ProteinsNestinSostdc1 protein, mouseSp7 protein, mouseSp7 Transcription FactorBone regenerationEctodinFracture repairPeriosteumSostSostdc1Sost-likeUsag-1WiseWnt signaling

Identifiers

PMID27102547
PMCPMC6277141
OpenAlexW2339457409

What OpenQuestion holds

Textmetadata
LicenceTDM
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.