Evidence map›Paper›PMID 21266510›Full record

ArticleEndocrinology2011

β2-Adrenergic receptor signaling in osteoblasts contributes to the catabolic effect of glucocorticoids on bone.

Yun Ma, Jeffry S Nyman, Huan Tao, Heather H Moss, Xiangli Yang, Florent Elefteriou

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 8% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. β-Adrenergic receptor antagonists and fracture risk: a meta-analysis of selectivity, gender, and site-specific effects.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2014
    Pooled it
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  16. Cannabidiol for musculoskeletal regenerative medicine.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  17. The Sympathetic Nervous System in Dental Implantology.Journal of clinical medicine · 2023
    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

6 authors at 1 institution in 1 country.

Yun MaDepartment of Medicine, Vanderbilt University, 2215 Garland Avenue, MRB IV, Room 1225E, Nashville, Tennessee 37232-0575, USA.
Jeffry S Nyman
Huan Tao
Heather H Moss
Xiangli Yang
Florent Elefteriou
Vanderbilt University Medical Center · US

Funding

Transcriptional Regulation of Indian Hedgehog Expression in ChondrocytesR01AR055972 · NIAMS · VANDERBILT UNIVERSITY · PI YANG, XIANGLI · 2008 to 2012
$1.7M
Glucocorticoid-induced bone loss via Beta2-adrenergic signaling in osteoblastsR21DK074994 · NIDDK · VANDERBILT UNIVERSITY · PI ELEFTERIOU, FLORENT · 2006 to 2007
$293k
NIAMS NIH HHS R01 AR055972NIDDK NIH HHS DK074994-01NIDDK NIH HHS R21 DK074994
6 · The paper itself

Abstract

The sympathetic nervous system is a physiological regulator of bone homeostasis. Autonomic nerves are indeed present in bone, bone cells express the β2-adrenergic receptors (β2AR), and pharmacological or genetic disruption of sympathetic outflow to bone induces bone gain in rodents. These recent findings implied that conditions that affect β2AR signaling in osteoblasts and/or sympathetic drive to bone may contribute to bone diseases. In this study, we show that dexamethasone stimulates the expression of the β2AR in differentiated primary calvarial osteoblasts, as measured by an increase in Adrβ2 mRNA and β2AR protein level after short-term dexamethasone treatment. Isoproterenol-induced cAMP accumulation and the expression of the β2AR target gene Rankl were also significantly increased after dexamethasone pretreatment, indicating that dexamethasone promotes the responsiveness of differentiated osteoblasts to adrenergic stimulation. These in vitro results led to the hypothesis that glucocorticoid-induced bone loss, provoked by increased endogenous or high-dose exogenous glucocorticoids given for the treatment of inflammatory diseases, might, at least in part, be mediated by increased sensitivity of bone-forming cells to the tonic inhibitory effect of sympathetic nerves on bone formation or their stimulatory effect on bone resorption. Supporting this hypothesis, both pharmacological and genetic β2AR blockade in mice significantly reduced the bone catabolic effect of high-dose prednisolone in vivo. This study emphasizes the importance of sympathetic nerves in the regulation of bone homeostasis and indicates that this neuroskeletal signaling axis can be modulated by hormones or drugs and contribute to enhance pathological bone loss.

Indexed as

AnimalsAnimals, NewbornBlotting, WesternBone and BonesCell DifferentiationCell LineCells, CulturedCyclic AMPDexamethasoneGlucocorticoidsMiceOsteoblastsPolymerase Chain ReactionPrednisoloneReceptors, Adrenergic, beta-2Signal TransductionCyclic AMPDexamethasoneGlucocorticoidsPrednisoloneReceptors, Adrenergic, beta-2

Identifiers

PMID21266510
PMCPMC3060633
OpenAlexW2156972609

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.