Evidence map›Paper›PMID 20814968›Full record

ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2011

Calpain-6, a target molecule of glucocorticoids, regulates osteoclastic bone resorption via cytoskeletal organization and microtubule acetylation.

Jung Min Hong, Steven L Teitelbaum, Tae-Ho Kim, F Patrick Ross, Shin-Yoon Kim, Hyun-Ju Kim

Abstract read
In one paragraph

Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2011. 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
–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

24 citing papers in PubMed.

  1. Potential Link Between a DisruptiveInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Calpain and Cardiometabolic Diseases.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. CAPN6 in disease: An emerging therapeutic target (Review).International journal of molecular medicine · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  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

6 authors.

Jung Min HongSkeletal Diseases Genome Research Center, Kyungpook National University Hospital, Daegu, Korea.
Steven L Teitelbaum
Tae-Ho Kim
F Patrick Ross
Shin-Yoon Kim
Hyun-Ju Kim

Funding

Mechanisms of RANKL Mediated Osteoclast ActivationR01AR032788 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 1987 to 2012
$6.6M
MECHANISMS OF AVB3 INTEGRIN MEDIATED BONE RESORPTIONR01AR046523 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2000 to 2009
$4.0M
Mechanisms of AVB3 Integrin Mediated Bone ResorptionR37AR046523 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2010 to 2019
$3.3M
MECHANISMS OF POLARIZED SECRETION BY BONE CELLSR01AR057037 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2009 to 2013
$1.6M
CDC 42 BIM AND THE OSTEOCLASTR01AR054618 · NIAMS · WASHINGTON UNIVERSITY · PI TEITELBAUM, STEVEN L · 2009 to 2010
$758k
NIAMS NIH HHS AR032788NIAMS NIH HHS AR046523NIAMS NIH HHS AR054618NIAMS NIH HHS AR057037NIAMS NIH HHS R01 AR032788NIAMS NIH HHS R01 AR046523NIAMS NIH HHS R01 AR054618NIAMS NIH HHS R01 AR057037NIAMS NIH HHS R37 AR046523
6 · The paper itself

Abstract

Glucocorticoids (GCs) inhibit the resorptive capacity of the osteoclast by disrupting its cytoskeleton. We find that calpain-6 (Capn6), a unique, nonproteolytic member of its family, is suppressed 12-fold by dexamethasone (DEX) in the bone-degrading cell. While Capn6 abundance parallels commitment of naive bone marrow macrophages (BMMs) to the osteoclast phenotype, its excess or deletion does not affect the cell's differentiation. On the other hand, Capn6 localizes to the sealing zone, and its overexpression promotes osteoclast spreading and large actin ring formation, eventuating in stimulated bone degradation. Conversely, Capn6 knockdown impairs cytoskeletal organization and the cell's resorptive capacity. Capn6 complexes with tubulin, and its absence inhibits microtubule acetylation and stability in the osteoclast. Knockdown of Capn6 also reduces β(3)-integrin subunit protein, another essential regulator of osteoclast cytoskeletal function. Reflecting Capn6 as a target molecule of GCs, microtubule stability and acetylation, as well as the expression of β(3)-integrin protein, are similarly suppressed in DEX-treated osteoclasts. Moreover, overexpression of Capn6 rescues GC-mediated disruption of osteoclast cytoskeleton. Thus Capn6 promotes cytoskeletal organization and microtubule stability in osteoclasts, and its inhibition may mediate the resorption-arresting properties of GCs.

Indexed as

AcetylationAnimalsBone ResorptionCalpainCell MovementCytoskeletonDexamethasoneGene Knockdown TechniquesGlucocorticoidsIntegrin beta3MiceMice, Inbred C57BLMicrotubulesOsteoclastsOsteogenesisUp-RegulationCalpainCapn6 protein, mouseDexamethasoneGlucocorticoidsIntegrin beta3

Identifiers

PMID20814968
PMCPMC3179291

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Registered trials

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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.