Evidence map›Paper›PMID 26082314›Full record

ArticleMolecular medicine reports2015

15-hydroxyprostaglandin dehydrogenase is upregulated by hydroxychloroquine in rheumatoid arthritis fibroblast-like synoviocytes.

Hak-Jae Kim, Sora Lee, Haw-Yong Lee, Hansol Won, Sung-Hae Chang, Seong-Su Nah

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07751263 (15-Hydroxyprostaglandin Dehydrogenase in Osteoarthritis and Ankylosing Spondylitis), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 30% 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.

NCT07751263 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

15-Hydroxyprostaglandin Dehydrogenase in Osteoarthritis and Ankylosing Spondylitis: Associations With Clinical and Musculoskeletal Ultrasound Features.

Typeobservational_patient_registrySponsorAssiut UniversityRan2026 to 2028Enrolled51ConditionsOsteoarthritis, Ankylosing Spondylitis
3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 13 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

6 authors at 1 institution in 1 country.

Hak-Jae KimDepartment of Clinical Pharmacology, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Sora LeeDivision of Rheumatology, Department of Internal Medicine, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Haw-Yong LeeDepartment of Clinical Pharmacology, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Hansol WonDepartment of Clinical Pharmacology, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Sung-Hae ChangDivision of Rheumatology, Department of Internal Medicine, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Seong-Su NahDivision of Rheumatology, Department of Internal Medicine, College of Medicine, Soonchunhyang University, Cheonan, Choongcheongnam-do 330-930, Republic of Korea.
Soonchunhyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

15-Hydroxyprostaglandin dehydrogenase (HPGD) is the key enzyme responsible for the metabolic inactivation of prostaglandin E2 (PGE2) catabolism. PGE2 is one of the predominant catabolic factors involved in rheumatoid arthritis (RA). However, the expression and regulation of HPGD in RA fibroblast‑like synoviocyte (FLS) remain to be elucidated. Disease‑modifying anti‑rheumatic drugs (DMARDs) are the most important anti‑arthritic drugs, which reduce the effect of joint injury. The aim of the present study was to assess the expression of HPGD in RA tissues and cells, and normal synovial tissues and cells. The effect of the most popular DMARDs, hydroxychloroquine, on the expression of HPGD in RA‑FLS was also investigated. Western blotting and immunohistochemical analysis demonstrated that the expression levels of HPGD in human synovium were lower in RA synovium compared with the normal and OA synovium. In RA‑FLS, the expression of HPGD was increased following treatment with several DMARDs, including sulfasalazine, methotrexate, and hydroxychloroquine. Hydroxychloroquine (10 µM) treatment induced the phosphorylation of ERK, SAPK/JNK and p38. Hydroxychloroquine induced a decrease in the release of PGE2, which was restored by mitogen‑activated protein (MAP) kinase pathway inhibitors. Hydroxychloroquine may therefore, affect the pathogenesis of RA through the MAP kinase pathway by regulating the expression of HPGD.

Indexed as

Arthritis, RheumatoidCells, CulturedFibroblastsHumansHydroxychloroquineHydroxyprostaglandin DehydrogenasesImmunohistochemistryMicroscopy, ConfocalMitogen-Activated Protein KinasesOsteoarthritisPhosphorylationSynovial MembraneUp-Regulation15-hydroxyprostaglandin dehydrogenaseHydroxychloroquineHydroxyprostaglandin DehydrogenasesMitogen-Activated Protein Kinases

Identifiers

PMID26082314
PMCPMC4526038
OpenAlexW2150704549

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Registered trials

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.