Evidence map›Paper›PMID 21897843›Full record

ArticlePloS one2011

Enhanced osteoclastic resorption and responsiveness to mechanical load in gap junction deficient bone.

Yue Zhang, Emmanuel M Paul, Vikram Sathyendra, Andrew Davison, Neil Sharkey, Sarah Bronson, Sundar Srinivasan, Ted S Gross, Henry J Donahue

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023
    Review
  10. The osteocyte and its osteoclastogenic potential.Frontiers in endocrinology · 2023
    Review
  11. Article
  12. Article
  13. Similarities Between Disuse and Age-Induced Bone Loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Connexin 43 Hemichannels Regulate Osteoblast to Osteocyte Differentiation.Frontiers in cell and developmental biology · 2022
    Article

37 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Yue ZhangDivision of Musculoskeletal Sciences, Department of Orthopaedics and Rehabilitation, Penn State College of Medicine, Hershey, Pennsylvania, United States of America.
Emmanuel M Paul
Vikram Sathyendra
Andrew Davison
Neil Sharkey
Sarah Bronson
Sundar Srinivasan
Ted S Gross
Henry J Donahue
Penn State Milton S. Hershey Medical Center · USUniversity of Washington · US

Funding

GAP JUNCTIONS AND BONE CELL RESPONSE TO PHYSICAL SIGNALSR01AG013087 · NIA · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI DONAHUE, HENRY J · 1994 to 2010
$2.5M
Osteoblastic lineage cells regulate osteoclastogenesis via Cx43 and gap junctionsR03AR057546 · NIAMS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI ZHANG, YUE · 2009 to 2011
$230k
NIAMS NIH HHS R03 AR057546NIAMS NIH HHS R03 AR057546-01NIA NIH HHS R01 AG013087NIA NIH HHS R01 AG013087-13
6 · The paper itself

Abstract

Emerging evidence suggests that connexin mediated gap junctional intercellular communication contributes to many aspects of bone biology including bone development, maintenance of bone homeostasis and responsiveness of bone cells to diverse extracellular signals. Deletion of connexin 43, the predominant gap junction protein in bone, is embryonic lethal making it challenging to examine the role of connexin 43 in bone in vivo. However, transgenic murine models in which only osteocytes and osteoblasts are deficient in connexin 43, and which are fully viable, have recently been developed. Unfortunately, the bone phenotype of different connexin 43 deficient models has been variable. To address this issue, we used an osteocalcin driven Cre-lox system to create osteoblast and osteocyte specific connexin 43 deficient mice. These mice displayed bone loss as a result of increased bone resorption and osteoclastogenesis. The mechanism underlying this increased osteoclastogenesis included increases in the osteocytic, but not osteoblastic, RANKL/OPG ratio. Previous in vitro studies suggest that connexin 43 deficient bone cells are less responsive to biomechanical signals. Interestingly, and in contrast to in vitro studies, we found that connexin 43 deficient mice displayed an enhanced anabolic response to mechanical load. Our results suggest that transient inhibition of connexin 43 expression and gap junctional intercellular communication may prove a potentially powerful means of enhancing the anabolic response of bone to mechanical loading.

Indexed as

Mechanical PhenomenaAnimalsBiomechanical PhenomenaBone and BonesBone DensityBone ResorptionCell CommunicationCell LineConnexin 43Gap JunctionsGene DeletionHumansMaleMiceOsteoclastsOsteocytesConnexin 43OsteoprotegerinRANK LigandRNA, MessengerTnfrsf11b protein, mouse

Identifiers

PMID21897843
PMCPMC3163577
OpenAlexW2022309828

What OpenQuestion holds

Textmetadata
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.