Evidence map›Paper›PMID 32736577›Full record

ArticleArthritis research & therapy2020

The role of the oncostatin M/OSM receptor β axis in activating dermal microvascular endothelial cells in systemic sclerosis.

G Marden, Q Wan, J Wilks, K Nevin, M Feeney, N Wisniacki, M Trojanowski, A Bujor, L Stawski, M Trojanowska

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Epigenetic Modifications in the Pathogenesis of Systemic Sclerosis.International journal of general medicine · 2022
    Review
  16. Review
  17. Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021
    Review
  18. 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

10 authors at 2 institutions in 3 countries.

G MardenArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
Q WanArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
J WilksArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
K NevinImmuno-Inflammation Therapeutic Area Unit, GlaxoSmithKline, Stevenage, UK.
M FeeneyImmuno-Inflammation Therapeutic Area Unit, GlaxoSmithKline, Stevenage, UK.
N WisniackiImmuno-Inflammation Therapeutic Area Unit, GlaxoSmithKline, Stevenage, UK.
M TrojanowskiArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
A BujorArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
L StawskiArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA.
M TrojanowskaArthritis Centre, Boston University School of Medicine, Boston University, 72 East Concord St, E-5, Boston, MA, 02118, USA. trojanme@bu.edu.ORCID 0000-0001-9550-7178
Boston University · USGlaxoSmithKline (United Kingdom) · GB

Funding

TGF BETA RECEPTOR SIGNALING IN SCLERODERMAR01AR044883 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2012
$3.3M
TGF-beta receptor/Endoglin signaling and the origin of scleroderma fibroblastR56AR044883 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TROJANOWSKA, MARIA · 2015 to 2015
$410k
NIAMS NIH HHS AR44883NIAMS NIH HHS R01 AR044883NIAMS NIH HHS R56 AR044883
6 · The paper itself

Abstract

backgroundScleroderma (SSc) is a rare autoimmune disease characterized by vascular impairment and progressive fibrosis of the skin and other organs. Oncostatin M, a member of the IL-6 family, is elevated in SSc serum and was recognized as a significant player in various stages of fibrosis. The goal of this study was to assess the contribution of the OSM/OSMRβ pathway to endothelial cell (EC) injury and activation in SSc.

methodsIHC and IF were used to assess the distribution of OSM and OSMRβ in SSc (n = 14) and healthy control (n = 7) skin biopsies. Cell culture experiments were performed in human dermal microvascular endothelial cells (HDMECs) and included mRNA and protein analysis, and cell migration and proliferation assays. Ex vivo skin organoid culture was used to evaluate the effect of OSM on perivascular fibrosis.

resultsOSMRβ protein was elevated in dermal ECs and in fibroblasts of SSc patients. Treatments of HDMECs with OSM or IL-6+sIL-6R have demonstrated that both cytokines similarly stimulated proinflammatory genes and genes related to endothelial to mesenchymal transition (EndMT). OSM was more effective than IL-6+sIL-6R in inducing cell migration, while both treatments similarly induced cell proliferation. The effects of OSM were mediated via OSMRβ and STAT3, while the LIFR did not contribute to these responses. Both OSM and IL-6+sIL-6R induced profibrotic gene expression in HDMECs, as well as expansion of the perivascular PDGFRβ

conclusionsThis work provides new insights into the role of the OSM/OSMRβ axis in activation/injury of dermal ECs and supports the involvement of this pathway in SSc vascular disease.

Indexed as

Oncostatin M Receptor beta SubunitScleroderma, SystemicEndothelial CellsFibrosisHumansOncostatin MOncostatin MOncostatin M Receptor beta SubunitOSM protein, humanEndothelial cellsERGFLI1IL-6OSMOSMRβSSc

Identifiers

PMID32736577
PMCPMC7393919
OpenAlexW3046521658

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.