Evidence map›Paper›PMID 33042430›Full record

ArticleAmerican journal of translational research2020

LncRNA TUG1 promotes the intervertebral disc degeneration and nucleus pulposus cell apoptosis though modulating miR-26a/HMGB1 axis and regulating NF-κB activation.

Ning Tang, Yulei Dong, Tinghui Xiao, Hong Zhao

Abstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  8. Association betweenCell cycle (Georgetown, Tex.) · 2022
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  10. [Effect of resveratrol on high mobility group box-1 protein signaling pathway in cartilage endplate degeneration caused by inflammation].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022
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  20. hsa-miR-508-5p as a New Potential Player in Intervertebral Disc Degeneration.International journal of molecular and cellular medicine · 2022
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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

4 authors.

Ning TangDepartment of Orthopedic, Chinese Academy of Medical Sciences Peking Union Medical College Hospital Beijing, China.
Yulei DongDepartment of Orthopedic, Chinese Academy of Medical Sciences Peking Union Medical College Hospital Beijing, China.
Tinghui XiaoDepartment of Orthopedic, Shenzhen People's Hospital First Affiliated Hospital of Southern University of Science and Technology Shenzhen, China.
Hong ZhaoDepartment of Orthopedic, Chinese Academy of Medical Sciences Peking Union Medical College Hospital Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThis study was to investigate the effect of TUG1 on apoptosis and ECM degradation of human degenerative intervertebral disc nucleus pulposus cells (NPCs) and its mechanism.

methodsHuman degenerative intervertebral disc NP tissues were obtained from 10 patients with lumbar disc herniation (LDH) who underwent lumbar spine surgery (IDD group), normal intervertebral disc NP tissues were obtained from 10 patients with lumbar vertebrae fractures (LVF group).

resultsThe expression of TUG1 and HMGB1 protein in human degenerative disc NP tissues and NPCs was significantly increased, while the level of miR-26a was significantly decreased. Overexpression of TUG1 inhibited the proliferation while promoted apoptosis and ECM degradation of human degenerative intervertebral disc NPCs. Simultaneously, the effect of TUG1 knockdown on NPCs was opposite. Interestingly, TUG1 acted as an endogenous sponge to down-regulate the expression of miR-26a in NPCs by direct binding to miR-26a. Overexpression of miR-26a reversed the effects of TUG1 overexpression on apoptosis and ECM degradation. Additionally, HMGB1 was a target gene of miR-26a. The increased expression of HMGB1 induced by TUG1 overexpression could be reversed by the introduction of miR-26a mimic. Overexpression of TUG1 significantly upregulated the expression of p65 in the nucleus, while overexpression of TUG1 partially abolished the inhibition of NF-κB by QNZ pretreatment.

conclusionTUG1 could promote the apoptosis and ECM degradation of degenerated intervertebral disc NPCs by regulating the miR-26a/HMGB1, which may be involved in the activation of NF-κB pathway.

Indexed as

apoptosisextracellular matrix degradationIntervertebral disc degenerationlong-chain non-coding RNAs taurine upregulated gene 1nucleus pulposus cells

Identifiers

PMID33042430
PMCPMC7540166

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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.