Evidence map›Paper›PMID 28970490›Full record

ArticleScientific reports2017

Mast Cell-Intervertebral disc cell interactions regulate inflammation, catabolism and angiogenesis in Discogenic Back Pain.

Matthew G Wiet, Andrew Piscioneri, Safdar N Khan, Megan N Ballinger, Judith A Hoyland, Devina Purmessur

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.1field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Journal of orthopaedic translation · 2025
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  17. The JNK signaling pathway in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024
    Review
  18. Article
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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 3 institutions in 2 countries.

Matthew G WietDepartment of Biomedical Engineering, The Ohio State University, Columbus Ohio, 201 Davis Heart and Lung Research Institute, 473 W 12th Avenue, Columbus, Ohio, 43210, USA.
Andrew PiscioneriDepartment of Biomedical Engineering, The Ohio State University, Columbus Ohio, 201 Davis Heart and Lung Research Institute, 473 W 12th Avenue, Columbus, Ohio, 43210, USA.
Safdar N KhanDepartment of Orthopedics, The Ohio State University Wexner Medical Center, 1070 OSU CarePoint East, 543 Taylor Avenue, Columbus, Ohio, 43203, USA.
Megan N BallingerDepartment of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, The Ohio State University, 201 Davis Heart and Lung Research Institute, 473 West 12th Avenue, Columbus, Ohio, 43210, USA.
Judith A HoylandDivision of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Stopford Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
Devina PurmessurDepartment of Biomedical Engineering, The Ohio State University, Columbus Ohio, 201 Davis Heart and Lung Research Institute, 473 W 12th Avenue, Columbus, Ohio, 43210, USA. devina.purmessur@osumc.edu.
The Ohio State University · USThe Ohio State University Wexner Medical Center · USHenry Royce Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low back pain (LBP) is a widespread debilitating disorder of significant socio-economic importance and intervertebral disc (IVD) degeneration has been implicated in its pathogenesis. Despite its high prevalence the underlying causes of LBP and IVD degeneration are not well understood. Recent work in musculoskeletal degenerative diseases such as osteoarthritis have revealed a critical role for immune cells, specifically mast cells in their pathophysiology, eluding to a potential role for these cells in the pathogenesis of IVD degeneration. This study sought to characterize the presence and role of mast cells within the IVD, specifically, mast cell-IVD cell interactions using immunohistochemistry and 3D in-vitro cell culture methods. Mast cells were upregulated in painful human IVD tissue and induced an inflammatory, catabolic and pro-angiogenic phenotype in bovine nucleus pulposus and cartilage endplate cells at the gene level. Healthy bovine annulus fibrosus cells, however, demonstrated a protective role against key inflammatory (IL-1β and TNFα) and pro-angiogenic (VEGFA) genes expressed by mast cells, and mitigated neo-angiogenesis formation in vitro. In conclusion, mast cells can infiltrate and elicit a degenerate phenotype in IVD cells, enhancing key disease processes that characterize the degenerate IVD, making them a potential therapeutic target for LBP.

Indexed as

AdultAgedAnimalsAnnulus FibrosusCattleCell CommunicationCell LineChondrocytesFemaleGene Expression RegulationHumansInterleukin-1betaIntervertebral Disc DegenerationLow Back PainMaleMast CellsIL1B protein, humanInterleukin-1betaTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID28970490
PMCPMC5624870
OpenAlexW2756641402

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.