Evidence map›Paper›PMID 30923232›Full record

ArticleAnnals of the rheumatic diseases2019

CircSERPINE2 protects against osteoarthritis by targeting miR-1271 and ETS-related gene.

Shuying Shen, Yizheng Wu, Junxin Chen, Ziang Xie, Kangmao Huang, Gangliang Wang, Yute Yang, Weiyu Ni, Zhijun Chen, Peihua Shi and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed, 1 pooled it
15.6field-weighted citation impact, top 1% 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

174 citing papers in PubMed, 1 synthesis or guideline pooled it, 298 citations in OpenAlex.

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114 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

12 authors at 1 institution in 1 country.

Shuying Shen *Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Yizheng Wu *Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Junxin Chen *Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Ziang XieDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Kangmao HuangDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Gangliang WangDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Yute YangDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Weiyu NiDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Zhijun ChenDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Peihua ShiDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China.
Yan MaDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China 0099203@zju.edu.cn zjumayan@zju.edu.cn.
Shunwu FanDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University school of medicine & KeyLaboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang, Hangzhou 310016, China 0099203@zju.edu.cn zjumayan@zju.edu.cn.ORCID 0000-0002-8785-0280
Sir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesCircular RNAs (circRNA) expression aberration has been identified in various human diseases. In this study, we investigated whether circRNAs could act as competing endogenous RNAs to regulate the pathological process of osteoarthritis (OA).

methodsCircRNA deep sequencing was performed to the expression of circRNAs between OA and control cartilage tissues. The regulatory and functional role of CircSERPINE2 upregulation was examined in OA and was validated in vitro and in vivo, downstream target of CircSERPINE2 was explored. RNA pull down, a luciferase reporter assay, biotin-coupled microRNA capture and fluorescence in situ hybridisation were used to evaluate the interaction between CircSERPINE2 and miR-1271-5 p, as well as the target mRNA, E26 transformation-specific-related gene (ERG). The role and mechanism of CircSERPINE2 in OA was also explored in rabbit models.

resultsThe decreased expression of CircSERPINE2 in the OA cartilage tissues was directly associated with excessive apoptosis and imbalance between anabolic and catabolic factors of extracellular matrix (ECM). Mechanistically, CircSERPINE2 acted as a sponge of miR-1271-5 p and functioned in human chondrocytes (HCs) through targeting miR-1271-5 p and ERG. Intra-articular injection of adeno-associated virus-CircSERPINE2-wt alleviated OA in the rabbit model.

conclusionsOur results reveal an important role for a novel circRNA-CircSERPINE2 in OA progression. CircSERPINE2 overexpression could alleviate HCs apoptosis and promote anabolism of ECM through miR-1271-ERG pathway. It provides a potentially effective therapeutic strategy for OA progression.

Indexed as

AnimalsApoptosisArthritis, ExperimentalCartilage, ArticularCase-Control StudiesCell LineCells, CulturedChondrocytesExtracellular MatrixFemaleGene TargetingGenetic TherapyHumansMaleMicroRNAsMolecular Targeted TherapyMicroRNAsMIRN1271 microRNA, humanRNA, CircularSerpin E2SERPINE2 protein, humanchondrocytesknee osteoarthritisosteoarthritis

Identifiers

PMID30923232
PMCPMC6579553
OpenAlexW2933413627

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.