Evidence map›Paper›PMID 37542341›Full record

ArticleArthritis research & therapy2023

Transgenic disruption of endogenous glucocorticoid signaling in osteoblasts does not alter long-term K/BxN serum transfer-induced arthritis.

Tazio Maleitzke, Edgar Wiebe, Dörte Huscher, Cornelia M Spies, Jinwen Tu, Timo Gaber, Yu Zheng, Frank Buttgereit, Markus J Seibel, Hong Zhou

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

Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 79% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 2 countries.

Tazio Maleitzke *Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0003-2924-7384
Edgar Wiebe *Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia. edgar.wiebe@charite.de.ORCID http://orcid.org/0000-0002-3600-0788
Dörte HuscherInstitute of Biometry and Clinical Epidemiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin Institute of Health, Berlin, Germany.ORCID http://orcid.org/0000-0001-9070-0761
Cornelia M SpiesBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0001-6325-7418
Jinwen TuBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0003-2718-499X
Timo GaberDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-6675-3895
Yu ZhengBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-6324-8148
Frank ButtgereitDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-2534-550X
Markus J SeibelBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-2701-378X
Hong ZhouBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0001-5899-9660
The University of Sydney · AUHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisruption of glucocorticoid (GC) signaling in osteoblasts results in a marked attenuation of acute antibody-induced arthritis. The role of endogenous GCs in chronic inflammatory arthritis is however not fully understood. Here, we investigated the impact of endogenous GC signaling in osteoblasts on inflammation and bone integrity under chronic inflammatory arthritis by inactivating osteoblastic GC signaling in a long-term K/BxN serum transfer-induced induced arthritis (STIA) model.

methodsIntracellular GC signaling in osteoblasts was disrupted by transgenic (tg) overexpression of 11beta-hydroxysteroid dehydrogenase type 2 (11ß-HSD2). Inflammatory arthritis was induced in 5-week-old male tg mice and their wild type (WT) littermates by intraperitoneal (i.p.) injection of K/BxN serum while controls (CTRLs) received phosphate-buffered saline (PBS). In a first cohort, K/BxN STIA was allowed to abate until  the endpoint of 42 days (STIA). To mimic rheumatic flares, a second cohort was additionally injected on days 14 and 28 with K/BxN serum (STIA

resultsAcute arthritis developed in both tg and WT mice (STIA and STIA

conclusionsIn contrast to the previously reported modulating effects of endogenous GC signaling in osteoblasts during acute K/BxN STIA, this effect seems to perish during the chronic inflammatory and resolution phase. These findings indicate that endogenous GC signaling in osteoblasts may mainly be relevant during acute and subacute inflammatory processes.

Indexed as

ArthritisArthritis, ExperimentalAnimalsGlucocorticoidsInflammationMaleMiceMice, TransgenicOsteoblastsX-Ray MicrotomographyGlucocorticoids11ß-HSD2AntibodyBoneCartilageCortisolCortisoneJoint inflammationRheumatoid arthritis

Identifiers

PMID37542341
PMCPMC10401869
OpenAlexW4385581123

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.