Evidence map›Paper›PMID 26348666›Full record

ArticleBone2015

Hedgehog signaling mediates woven bone formation and vascularization during stress fracture healing.

Nikolas H Kazmers, Jennifer A McKenzie, Tony S Shen, Fanxin Long, 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  5. Article
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  7. International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Heterotopic ossification of tendon and ligament.Journal of cellular and molecular medicine · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Activation of hedgehog signaling by systemic agonist improves fracture healing in aged mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Nikolas H KazmersDepartment of Orthopaedic Surgery, Washington University, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: nkazmers@gmail.com.
Jennifer A McKenzieDepartment of Orthopaedic Surgery, Washington University, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Tony S ShenDepartment of Orthopaedic Surgery, Washington University, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Fanxin LongDepartment of Orthopaedic Surgery, Washington University, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110, USA; Department of Medicine, Washington University, St. Louis, MO, USA; Department of Developmental Biology, Washington University, St. Louis, MO, USA.
Matthew J SilvaDepartment of Orthopaedic Surgery, Washington University, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110, USA; Department of Biomedical Engineering, Washington University, St. Louis, MO, USA.
Washington University in St. Louis · US

Funding

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
INDIAN HEDGEHOG SIGNALING IN OSTEOBLAST DIFFERENTIATIONR01DK065789 · NIDDK · WASHINGTON UNIVERSITY · PI LONG, FANXIN · 2004 to 2013
$3.4M
WHOLE SLIDE IMAGING SYSTEM FOR TRANSLATIONAL NEUROSCIENCES10RR027552 · NCRR · WASHINGTON UNIVERSITY · PI LEE, JIN-MOO · 2010 to 2010
$275k
NCRR NIH HHS 1S10RR027552NCRR NIH HHS S10 RR027552NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR050211NIDDK NIH HHS R01 DK065789
6 · The paper itself

Abstract

Hedgehog (Hh) signaling is critical in developmental osteogenesis, and recent studies suggest it may also play a role in regulating osteogenic gene expression in the post-natal setting. However, there is a void of studies directly assessing the effect of Hh inhibition on post-natal osteogenesis. This study utilized a cyclic loading-induced ulnar stress fracture model to evaluate the hypothesis that Hh signaling contributes to osteogenesis and angiogenesis during stress fracture healing. Immediately prior to loading, adult rats were given GDC-0449 (Vismodegib - a selective Hh pathway inhibitor; 50mg/kg orally twice daily), or vehicle. Hh signaling was upregulated in response to stress fracture at 3 days (Ptch1, Gli1 expression), and was markedly inhibited by GDC-0449 at 1 day and 3 days in the loaded and non-loaded ulnae. GDC-0449 did not affect Hh ligand expression (Shh, Ihh, Dhh) at 1 day, but decreased Shh expression by 37% at 3 days. GDC-0449 decreased woven bone volume (-37%) and mineral density (-17%) at 7 days. Dynamic histomorphometry revealed that the 7 day callus was composed predominantly of woven bone in both groups. The observed reduction in woven bone occurred concomitantly with decreased expression of Alpl and Ibsp, but was not associated with differences in early cellular proliferation (as determined by callus PCNA staining at 3 days), osteoblastic differentiation (Osx expression at 1 day and 3 days), chondrogenic gene expression (Acan, Sox9, and Col2α1 expression at 1 day and 3 days), or bone resorption metrics (callus TRAP staining at 3 days, Rankl and Opg expression at 1 day and 3 days). To evaluate angiogenesis, vWF immunohistochemistry showed that GDC-0449 reduced fracture callus blood vessel density by 55% at 3 days, which was associated with increased Hif1α gene expression (+30%). Dynamic histomorphometric analysis demonstrated that GDC-0449 also inhibited lamellar bone formation. Lamellar bone analysis of the loaded limb (directly adjacent to the woven bone callus) showed that GDC-0449 significantly decreased mineral apposition rate (MAR) and bone formation rate (BFR/BS) (-17% and -20%, respectively). Lamellar BFR/BS in the non-loaded ulna was also significantly decreased (-37%), indicating that Hh signaling was required for normal bone modeling. In conclusion, Hh signaling plays an important role in post-natal osteogenesis in the setting of stress fracture healing, mediating its effects directly through regulation of bone formation and angiogenesis.

Indexed as

Neovascularization, PhysiologicAnilidesAnimalsBone ResorptionCell ProliferationFracture HealingFractures, StressHedgehog ProteinsMaleOsteogenesisPyridinesRatsRats, Inbred F344Signal TransductionUp-RegulationAnilidesHedgehog ProteinsHhAntag691PyridinesShh protein, ratAngiogenesisFracture healingHedgehogOsteogenesisWoven bone

Identifiers

PMID26348666
PMCPMC4640972
OpenAlexW2127518815

What OpenQuestion holds

Textmetadata
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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.