Evidence map›Paper›PMID 40677708›Full record

ArticleFrontiers in immunology2025

Oncostatin M enhances the lengthening of sensory nerves and skin hypersensitivity.

Chie Ishikawa, Ryo Saito, Masataka Suehiro, Kaori Ishii, Yuhki Yanase, Tomoko Kawaguchi, Kazue Uchida, Nozomi Yanagida, Tomofumi Numata, Wataru Sasaki and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
  2. Article
  3. 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

13 authors.

Chie IshikawaDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Ryo SaitoDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Masataka SuehiroDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kaori IshiiDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuhki YanaseDepartment of Pharmacotherapy, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tomoko KawaguchiDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazue UchidaDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Nozomi YanagidaDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tomofumi NumataDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Wataru SasakiDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Rina KamigakiDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Sachio TakenoDepartment of Otorhinolaryngology, Head and Neck Surgery, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Akio TanakaDepartment of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Oncostatin M (OSM) is a cytokine that mediates inflammatory processes and is overexpressed in skin lesions of atopic dermatitis (AD). By amplifying neural responses to chemicals such as histamine, OSM increases sensitivity to pruritus. However, the morphological effects of OSM on peripheral sensory nerves and their subsequent impact on pruritus remain unclear. This study investigated OSM-induced peripheral nerve elongation, which may contribute to skin hypersensitivity. Methods: We assessed neurite outgrowth using primary mouse dorsal root ganglion (DRG) cells treated with OSM, IL-31, or nerve growth factor. Next, we pre-treated the cells with inhibitors of downstream signaling pathways of OSM, including extracellular signal-regulated kinase (ERK), signal transducers and activator of transcription (STAT) 3, c-Jun N-terminal kinase (JNK), and p38, followed by OSM administration to measure neurite outgrowth. Furthermore, OSM receptor β-overexpressing cell lines were established by gene transfer into the DRG cell line, and nerve elongation was measured after OSM administration. Results: OSM significantly induced neurite outgrowth in DRG cells and the effect of OSM surpassed the effects of IL-31 and nerve growth factor. The neurite outgrowth effect of OSM involved the JAK/STAT3, MEK/ERK, and p38/MAPK pathways. Compared to control cells, DRG cell lines that overexpressed OSM receptor β showed significantly enhanced neurite outgrowth upon OSM treatment. Conclusion: OSM induces neurite elongation and may contribute to skin hypersensitivity. This suggests the potential utilization of OSM as a therapeutic target for inflammatory skin diseases such as AD.

Indexed as

Dermatitis, AtopicOncostatin MPruritusSensory Receptor CellsSkinAnimalsDisease Models, AnimalGanglia, SpinalHumansMaleMiceMice, Inbred C57BLNeuronal OutgrowthOncostatin M Receptor beta SubunitSignal TransductionOncostatin MOncostatin M Receptor beta Subunitatopic dermatitisitchnerve elongationoncostatin Mpruritussensory nerve

Identifiers

PMID40677708
PMCPMC12267034

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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.