Evidence map›Paper›PMID 33488928›Full record

ArticleOxidative medicine and cellular longevity2020

Exosomes Derived from Human Urine-Derived Stem Cells Inhibit Intervertebral Disc Degeneration by Ameliorating Endoplasmic Reticulum Stress.

HongFei Xiang, WeiLiang Su, XiaoLin Wu, WuJun Chen, WenBin Cong, Shuai Yang, Chang Liu, ChenSheng Qiu, Shang-You Yang, Yan Wang and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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  8. [Mechanism of extracellular vesicles in the repair of intervertebral disc degeneration].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2025
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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

14 authors at 1 institution in 2 countries.

HongFei XiangDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-5026-5918
WeiLiang SuDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0003-0784-8971
XiaoLin WuDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-6200-7000
WuJun ChenCancer Institute, The Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-1256-3201
WenBin CongRadiology Department, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0001-6288-1972
Shuai YangDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0003-1933-4484
Chang LiuDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0003-3085-4202
ChenSheng QiuDepartment of Orthopedics, Qingdao Municipal Hospital, Qingdao, Shandong 266011, China.ORCID https://orcid.org/0000-0002-0973-9026
Shang-You YangUniversity of Kansas, School of Medicine-Wichita, 929 N St. Francis Street, Wichita, KS, USA 67230.ORCID https://orcid.org/0000-0002-8835-5302
Yan WangDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-6460-9160
GuoQing ZhangDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-7539-2024
Zhu GuoDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-6044-5357
DongMing XingCancer Institute, The Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-2359-0440
BoHua ChenDepartment of Orthopedics, The Affiliated Hospital of Qingdao University, Qingdao, China 266003.ORCID https://orcid.org/0000-0002-5400-4352
Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study is aimed at determining the effects of human urine-derived stem cell-derived exosomes (USCs-exos) on pressure-induced nucleus pulposus cell (NPC) apoptosis and intervertebral disc degeneration (IDD) and on the ERK and AKT signaling pathways.

methodsThe NPCs were obtained from patients with herniated lumbar discs. Western blot analysis (WB) and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine endoplasmic reticulum (ER) stress levels of NPCs under stress. Human USCs were identified using an inverted microscope, three-line differentiation experiments, and flow cytometry. A transmission microscope, nanoparticle size analysis, and WB procedures were used to identify the extracted exosomes and observe NPC uptake. A control group, a 48 h group, and a USCs-exos group were established. The control group was untreated, and the 48 h group was pressure-trained for 48 h, while the USCs-exos group was pressure-trained for 48 h and treated with USCs-exos. WB, qRT-PCR, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis were used to determine the ER stress levels in stress conditions and after exosomal treatment. The AKT and ERK pathways were partially detected. Magnetic Resonance Imaging (MRI) and computed tomography (CT) were used to evaluate cell degeneration while exosomal effects on the intervertebral disc (IVD) tissue were determined by hematoxylin and eosin (HE) staining, Safranin O-fast green staining, immunohistochemical staining (IHC), nuclear magnetic resonance (NMR), spectrometric detection, and total correlation spectroscopy (TOCSY). IVD metabolites were also identified and quantified.

resultsAfter pressure culture, ER stress markers (GRP78 and C/EBP homologous protein (CHOP)) in the NPCs were significantly elevated with time (

conclusionThrough the AKT and ERK signaling pathways, USCs-exos significantly inhibit ER stress-induced cell apoptosis and IDD under pressure conditions. It is, therefore, a viable therapeutic strategy.

Indexed as

ApoptosisEndoplasmic Reticulum StressAdultAnimalsCell DifferentiationEndoplasmic Reticulum Chaperone BiPExosomesHumansIntervertebral Disc DegenerationMaleNucleus PulposusRats, Sprague-DawleySignal TransductionStem CellsUnfolded Protein ResponseUrineEndoplasmic Reticulum Chaperone BiP

Identifiers

PMID33488928
PMCPMC7787770
OpenAlexW3112517548

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.