Evidence map›Paper›PMID 26988982›Full record

ArticleJournal of translational medicine2016

IL-17 mediates inflammatory reactions via p38/c-Fos and JNK/c-Jun activation in an AP-1-dependent manner in human nucleus pulposus cells.

Jing-kun Li, Lin Nie, Yun-peng Zhao, Yuan-qiang Zhang, Xiaoqing Wang, Shuai-shuai Wang, Yi Liu, Hua Zhao, Lei Cheng

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Gut microbes · 2026
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23 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Jing-kun LiDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Lin NieDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Yun-peng ZhaoDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Yuan-qiang ZhangDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Xiaoqing WangDepartment of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai, 200011, People's Republic of China.
Shuai-shuai WangDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Yi LiuDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Hua ZhaoDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Lei ChengDepartment of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China. chengleiyx@126.com.
Qilu Hospital of Shandong University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow back pain and sciatica caused by intervertebral disc (IVD) disease are associated with inflammatory responses. The cytokine interleukin 17 (IL-17) is elevated in herniated and degenerated IVD tissues and acts as a regulator of disc inflammation. The objective of this study was to investigate the involvement of IL-17A in IVD inflammatory response and to explore the mechanisms underlying this response.

methodsCells were isolated from nucleus pulposus (NP) tissues collected from patients undergoing surgeries for IVD degeneration. The concentrations of COX2 and PGE2, as well as of select proteins involved in the mitogen-activated protein kinase (MAPK)/activating protein-1 (AP-1) pathway, were quantified in NP cells after exposure to IL-17 with or without pretreatment with MAPK or AP-1 inhibitors.

resultsOur results showed that IL-17A increased COX2 expression and PGE2 production via the activation of MAPKs, including p38 kinase and Jun N-terminal kinase (JNK). Moreover, IL-17A-induced COX2 and PGE2 production was shown to rely on p38/c-Fos and JNK/c-Jun activation in an AP-1-dependent manner.

conclusionIn summary, our results indicate that IL-17A enhances COX2 expression and PGE2 production via the p38/c-Fos and JNK/c-Jun signalling pathways in NP cells to mediate IVD inflammation.

Indexed as

AdultCells, CulturedCyclooxygenase 2DinoprostoneEnzyme ActivationFemaleHumansInflammationInterleukin-17Intervertebral DiscJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMiddle AgedModels, Biologicalp38 Mitogen-Activated Protein KinasesCyclooxygenase 2DinoprostoneInterleukin-17JNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-fosPTGS2 protein, humanTranscription Factor AP-1AP-1COX2IL-17LBPMAPKPGE2

Identifiers

PMID26988982
PMCPMC4794827
OpenAlexW2300803450

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.