Evidence map›Paper›PMID 26431344›Full record

ArticlePloS one2015

Sympathetic Neurotransmitters Modulate Osteoclastogenesis and Osteoclast Activity in the Context of Collagen-Induced Arthritis.

Dominique Muschter, Nicole Schäfer, Hubert Stangl, Rainer H Straub, Susanne Grässel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

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  8. [New insights into the function of bone marrow].Zeitschrift fur Rheumatologie · 2018
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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

5 authors at 1 institution in 1 country.

Dominique MuschterDepartment of Orthopedic Surgery, Experimental Orthopedics, University Hospital Regensburg, Regensburg, Bavaria, Germany; Center for Medical Biotechnology, BioPark I, Regensburg, Bavaria, Germany.
Nicole SchäferDepartment of Orthopedic Surgery, Experimental Orthopedics, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Hubert StanglDepartment of Internal Medicine I, Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Rainer H StraubDepartment of Internal Medicine I, Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Susanne GrässelDepartment of Orthopedic Surgery, Experimental Orthopedics, University Hospital Regensburg, Regensburg, Bavaria, Germany; Center for Medical Biotechnology, BioPark I, Regensburg, Bavaria, Germany.
University Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive synovial osteoclastogenesis is a hallmark of rheumatoid arthritis (RA). Concomitantly, local synovial changes comprise neuronal components of the peripheral sympathetic nervous system. Here, we wanted to analyze if collagen-induced arthritis (CIA) alters bone marrow-derived macrophage (BMM) osteoclastogenesis and osteoclast activity, and how sympathetic neurotransmitters participate in this process. Therefore, BMMs from Dark Agouti rats at different CIA stages were differentiated into osteoclasts in vitro and osteoclast number, cathepsin K activity, matrix resorption and apoptosis were analyzed in the presence of acetylcholine (ACh), noradrenaline (NA) vasoactive intestinal peptide (VIP) and assay-dependent, adenylyl cyclase activator NKH477. We observed modulation of neurotransmitter receptor mRNA expression in CIA osteoclasts without affecting protein level. CIA stage-dependently altered marker gene expression associated with osteoclast differentiation and activity without affecting osteoclast number or activity. Neurotransmitter stimulation modulated osteoclast differentiation, apoptosis and activity. VIP, NA and adenylyl cyclase activator NKH477 inhibited cathepsin K activity and osteoclastogenesis (NKH477, 10(-6) M NA) whereas ACh mostly acted pro-osteoclastogenic. We conclude that CIA alone does not affect metabolism of in vitro generated osteoclasts whereas stimulation with NA, VIP plus specific activation of adenylyl cyclase induced anti-resorptive effects probably mediated via cAMP signaling. Contrary, we suggest pro-osteoclastogenic and pro-resorptive properties of ACh mediated via muscarinic receptors.

Indexed as

AnimalsArthritis, ExperimentalCell DivisionCollagenNeurotransmitter AgentsOsteoclastsRatsCollagenNeurotransmitter Agents

Identifiers

PMID26431344
PMCPMC4592252
OpenAlexW2172612369

What OpenQuestion holds

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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.