Evidence map›Paper›PMID 30610061›Full record

ArticleAnnals of the rheumatic diseases2019

Critical role for arginase II in osteoarthritis pathogenesis.

Wan-Su Choi, Jeong-In Yang, Wihak Kim, Hyo-Eun Kim, Seul-Ki Kim, Yoonkyung Won, Young-Ok Son, Churl-Hong Chun, Jang-Soo Chun

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Effect of smoking on the redox status of knee osteoarthritis: A preliminary study.Experimental biology and medicine (Maywood, N.J.) · 2023
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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

9 authors at 3 institutions in 2 countries.

Wan-Su Choi *National Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Jeong-In Yang *National Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Wihak KimNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Hyo-Eun KimNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Seul-Ki KimNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Yoonkyung WonNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Young-Ok SonNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Churl-Hong ChunDepartment of Orthopedic Surgery, Wonkwang University School of Medicine, Iksan, Republic of Korea.
Jang-Soo ChunNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea jschun@gist.ac.kr.
Gwangju Institute of Science and Technology · KRCreative Research · GBWonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOsteoarthritis (OA) appears to be associated with various metabolic disorders, but the potential contribution of amino acid metabolism to OA pathogenesis has not been clearly elucidated. Here, we explored whether alterations in the amino acid metabolism of chondrocytes could regulate OA pathogenesis.

methodsExpression profiles of amino acid metabolism-regulating genes in primary-culture passage 0 mouse chondrocytes were examined by microarray analysis, and selected genes were further characterised in mouse OA chondrocytes and OA cartilage of human and mouse models. Experimental OA in mice was induced by destabilisation of the medial meniscus (DMM) or intra-articular (IA) injection of adenoviruses expressing catabolic regulators. The functional consequences of arginase II (Arg-II) were examined in

resultsThe gene encoding Arg-II, an arginine-metabolising enzyme, was specifically upregulated in chondrocytes under various pathological conditions and in OA cartilage from human patients with OA and various mouse models. Adenovirus-mediated overexpression of Arg-II in mouse joint tissues caused OA pathogenesis, whereas genetic ablation of

conclusionsOur results indicate that Arg-II is a crucial regulator of OA pathogenesis in mice. Although chondrocytes of human and mouse do not identically, but similarly, respond to Arg-II, our results suggest that Arg-II could be a therapeutic target of OA pathogenesis.

Indexed as

AnimalsArginaseArthritis, ExperimentalCartilage, ArticularChondrocytesDisease Models, AnimalHumansMatrix Metalloproteinase 13Matrix Metalloproteinase 3MiceOsteoarthritisUp-RegulationArg2 protein, mouseArginaseMatrix Metalloproteinase 13Matrix Metalloproteinase 3arginase IIcartilagechondrocytesmatrix metalloproteinasesosteoarthritis

Identifiers

PMID30610061
PMCPMC6390026
OpenAlexW2908321945

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.