Evidence map›Paper›PMID 29534600›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2018

The long non-coding RNA NEAT1 contributes to extracellular matrix degradation in degenerative human nucleus pulposus cells.

Zhi Ruan, Hui Ma, Jing Li, Huiyong Liu, Haoruo Jia, Feng Li

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  6. Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers.Journal of cell communication and signaling · 2023
    Review
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  9. Article
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  14. Review
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  17. HOXC13-AS Induced Extracellular Matrix LossFrontiers in molecular biosciences · 2021
    Article
  18. Review
  19. Review
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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 1 country.

Zhi Ruan1 Department of Orthopaedic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Hui Ma2 Department of Orthopaedic, First Affiliated Hospital, School of Medicine, Shihezi University, ShiHeZi, Xinjiang, China.
Jing Li2 Department of Orthopaedic, First Affiliated Hospital, School of Medicine, Shihezi University, ShiHeZi, Xinjiang, China.
Huiyong Liu1 Department of Orthopaedic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Haoruo Jia2 Department of Orthopaedic, First Affiliated Hospital, School of Medicine, Shihezi University, ShiHeZi, Xinjiang, China.
Feng Li1 Department of Orthopaedic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
First Affiliated Hospital of Shihezi University Medical College · CNTongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intervertebral disc degeneration is a complex disease involving genetic and environmental factors and multiple cellular processes. The role and expression of the lncRNA NEAT1 were assessed in intervertebral disc degeneration. NEAT1 expression was assessed in degenerative and control nucleus pulposus using RT-PCR. Western blotting and RT-PCR were also used to investigate p53 and p21 levels in nucleus pulposus tissues. NEAT1 function in degenerative nucleus pulposus cells was assessed with gain- and loss-of-function experiments. ERK/MAPK signaling was also examined. NEAT1, p53, and p21 were dramatically upregulated in intervertebral disc degeneration. Furthermore, catabolic MMP13 and ADAMTS5 were dysregulated and collagen II and aggrecan were downregulated after NEAT1 overexpression. This effect was reversed by transfection with si-NEAT1 in degenerative nucleus pulposus cells. In addition, NEAT1 was found to affect the activation of the ERK/MAPK pathway. The NEAT1-induced ECM degradation may involve ERK1/2/MAPK signaling. LncRNA NEAT1 may represent a novel molecular target for intervertebral disc degeneration treatment by preventing nucleus pulposus ECM degradation. Impact statement For the first time, our study demonstrates that lncRNA NEAT1 plays a role in the occurrence and development of IDD by participating in extracellular matrix remodeling. This lncRNA regulates catabolic MMP13 and ADAMTS5 and anabolic collagen II and aggrecan by affecting the ERK/MAPK signaling pathway in degenerative human nucleus pulposus (NP) cells. Our research provides a scientific basis for targeting of NEAT1 for the IDD.

Indexed as

AdolescentAdultCyclin-Dependent Kinase Inhibitor p21Extracellular MatrixFemaleHumansIntervertebral DiscIntervertebral Disc DegenerationMaleMAP Kinase Signaling SystemMiddle AgedMitogen-Activated Protein KinasesNucleus PulposusRNA, Long NoncodingSignal TransductionTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21Mitogen-Activated Protein KinasesNEAT1 long non-coding RNA, humanRNA, Long NoncodingTumor Suppressor Protein p53degenerationERK/MARKintervertebral discNEAT1nucleus pulposus cells

Identifiers

PMID29534600
PMCPMC6582394
OpenAlexW2793536219

What OpenQuestion holds

Textmetadata
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.