Evidence map›Paper›PMID 26750808›Full record

ArticleBritish journal of pharmacology2016

α1B -Adrenoceptor signalling regulates bone formation through the up-regulation of CCAAT/enhancer-binding protein δ expression in osteoblasts.

Kenjiro Tanaka, Takao Hirai, Daisuke Kodama, Hisataka Kondo, Kazunori Hamamura, Akifumi Togari

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Crosstalk between Bone and Nerves within Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  13. Driving βFrontiers in immunology · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 at 2 institutions in 1 country.

Kenjiro TanakaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Takao HiraiDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Daisuke KodamaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Hisataka KondoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Kazunori HamamuraDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Akifumi TogariDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Aichi Gakuin University · JPNagoya Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe sympathetic nervous system regulates bone remodelling, in part, through ß2 -adrenoceptor signalling. However, the physiological role of α1 -adrenoceptor signalling in bone in vivo remains unclear. Therefore, to obtain a deeper understanding of bone remodelling by the sympathetic nervous system, we investigated the role of α1B -adrenoceptor signalling in bone metabolism. EXPERIMENTAL APPROACH: Prazosin, a nonspecific α1 -adrenoceptor antagonist, was administered for 2 weeks in C57BL6 mice, and efficacy was evaluated by bone microarchitecture using microcomputed tomography and determination of bone formation by fluorescent labelling of bone. We also compared the bone phenotype of α1B -adrenoceptor null mice (α1B (-/-) ) with that of wild-type littermates. KEY

resultsWe demonstrated that the systemic administration of prazosin decreased bone formation. In addition, α1B -adrenoceptor-deficient mice had a lower bone mass due to decreased bone formation but did not exhibit any changes in bone-resorbing activity. Furthermore, stimulation with phenylephrine, a non-specific α1 -adrenoceptor agonist, increased the expression of the transcriptional factor CCAAT/enhancer-binding protein δ (Cebpd) in MC3T3-E1 osteoblastic cells. The overexpression of Cebpd induced cellular proliferation in MC3T3-E1 cells, whereas the silencing of Cebpd suppressed it. CONCLUSIONS AND IMPLICATIONS: Taken together, these results suggested that α1B -adrenoceptor signalling is required for bone formation and regulated cellular proliferation through a mechanism relevant to the up-regulation of Cebpd in osteoblasts and, thus, provide new evidence for the physiological importance of α1B -adrenoceptor signalling in bone homeostasis.

Indexed as

Adrenergic alpha-1 Receptor AgonistsAdrenergic alpha-1 Receptor AntagonistsAnimalsCCAAT-Enhancer-Binding Protein-deltaCell LineFemurMaleMice, Inbred C57BLMice, KnockoutOsteoblastsOsteogenesisPhenylephrinePrazosinReceptors, Adrenergic, alpha-1Signal TransductionUp-RegulationAdrenergic alpha-1 Receptor AgonistsAdrenergic alpha-1 Receptor AntagonistsCCAAT-Enhancer-Binding Protein-deltaPhenylephrinePrazosinReceptors, Adrenergic, alpha-1

Identifiers

PMID26750808
PMCPMC5341235
OpenAlexW2226709689

What OpenQuestion holds

Textmetadata
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.