Evidence map›Paper›PMID 33942704›Full record

ArticleBioengineered2021

Long non-coding RNA MCM3AP-AS1 protects chondrocytes ATDC5 and CHON-001 from IL-1β-induced inflammation via regulating miR-138-5p/SIRT1.

Jianming Shi, Fuyang Cao, Yingjian Chang, Chaofei Xin, Xu Jiang, Jianzhong Xu, Shitao Lu

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.0field-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

36 citing papers in PubMed, 39 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Jianming ShiDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Fuyang CaoDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yingjian ChangDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Chaofei XinDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xu JiangDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Jianzhong XuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.ORCID 0000-0002-5162-5137
Shitao LuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a chronic inflammatory joint disease. Increased apoptosis of chondrocytes contributes to cartilage degradation in OA pathogenesis. The function of lncRNA MCM3AP-AS1 in regulating the viability of chondrocytes still awaits further elaboration. In this work, MCM3AP-AS1, miR-138-5p and SIRT1 mRNA expression levels in OA and normal cartilage tissues were detected by qRT-PCR. Besides, chondrocyte cell lines, CHON-001 and ATDC5 induced by interleukin-1β (IL-1β) were used to initiate the inflammatory response environment of OA. CCK-8 assay was used to examine the cell multiplication; meanwhile, transwell assay was utilized to detect migration. Western blot was adopted to determine SIRT1 expression in chondrocyte. Enzyme-linked immunosorbent assay (ELISA) was performed to evaluate inflammatory factor levels. In addition, the binding sites between MCM3AP-AS1 and miR-138-5p, miR-138-5p and 3'UTR of SIRT1 were validated by dual-luciferase reporter assay, RIP assay or RNA pull-down assay. It was found that MCM3AP-AS1 was declined in OA cartilage tissues, positively interrelated with SIRT1 expression while negatively correlated with miR-138-5p. MCM3AP-AS1 up-regulation enhanced the viability and migration of CHON-001 and ATDC5 cells while restraining the apoptosis and inflammatory response. Additionally, miR-138-5p overexpression counteracted the effects on chondrocytes caused by MCM3AP-AS1 overexpression. MCM3AP-AS1 could adsorb miR-138-5p, and SIRT1 was verified as a target of miR-138-5p, and SIRT1 could be up-regulated by overexpression of MCM3AP-AS1 indirectly. In conclusion, MCM3AP-AS1 has the potential to be the 'ceRNA' to regulate miR-138-5p and SIRT1 in chondrocytes, and to participate in the pathogenesis of OA.

Indexed as

ChondrocytesCell LineFemaleHumansInflammationInterleukin-1betaMaleMicroRNAsMiddle AgedOsteoarthritisRNA, Long NoncodingSirtuin 1IL1B protein, humanInterleukin-1betaMicroRNAsMIRN138 microRNA, humanRNA, Long NoncodingSIRT1 protein, humanSirtuin 1MCM3AP-as1miR-138-5posteoarthritissirt1

Identifiers

PMID33942704
PMCPMC8806229
OpenAlexW3159315195

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.