Evidence map›Paper›PMID 25894998›Full record

ArticlePloS one2015

The effect of vascular endothelial growth factor on osteoclastogenesis in rheumatoid arthritis.

Hae-Rim Kim, Kyoung-Woon Kim, Bo-Mi Kim, Mi-La Cho, Sang-Heon Lee

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

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  19. Antirheumatoid Arthritic Effects ofFrontiers in pharmacology · 2022
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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

5 authors at 3 institutions in 1 country.

Hae-Rim KimDepartment of Rheumatology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, Korea.
Kyoung-Woon KimConversant Research Consortium in Immunologic disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea; The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea.
Bo-Mi KimConversant Research Consortium in Immunologic disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea; The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea.
Mi-La ChoConversant Research Consortium in Immunologic disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea; The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea.
Sang-Heon LeeDepartment of Rheumatology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, Korea.
Catholic University of Korea · KRKonkuk University · KRSeoul St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) has angiogenic, inflammatory, and bone-destructive roles in rheumatoid arthritis (RA). We aimed to determine the unique role of VEGF in osteoclastogenesis in RA. VEGF-induced receptor activator of nuclear factor ҡB ligand (RANKL) expression was determined in RA synovial fibroblasts by real-time PCR, luciferase assays, and ELISA. Osteoclastogenesis in peripheral blood monocytes cultured with VEGF was assessed by determining the numbers of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Synovial fluid RANKL was correlated with VEGF concentration in the RA patients. VEGF stimulated the expression of RANKL in RA synovial fibroblasts. The RANKL promoter activity was upregulated by VEGF in the synovial fibroblasts transfected with RANKL-reporter plasmids. The VEGF-induced RANKL expression was decreased by the inhibition of both VEGF receptors (VEGFR) 1 and 2, Src, protein kinase C (PKC) and p38 MAPK. VEGF induced osteoclast differentiation from monocytes in the absence of RANKL and this was decreased by the inhibition of VEGFR1 and 2, Src, PKC and p38 MAPK. On coculturing with VEGF-prestimulated RA synovial fibroblasts, the monocytes differentiated into osteoclasts, and the osteoclastogenesis decreased by inhibition of Src and PKC pathways. VEGF plays dual roles on osteoclastogenesis in RA: direct induction of osteoclastogenesis from the precursors and stimulation of RANKL production in synovial fibroblasts, which is mediated by Src and PKC pathways. The axis of VEGF and RANKL could be a potential therapeutic target for RA-associated bone destruction.

Indexed as

Arthritis, RheumatoidCell DifferentiationFemaleFibroblastsGene Expression RegulationHumansIntracellular SpaceMaleMiddle AgedMonocytesOsteoclastsRANK LigandSignal TransductionSynovial FluidVascular Endothelial Growth Factor ARANK LigandVascular Endothelial Growth Factor A

Identifiers

PMID25894998
PMCPMC4404365
OpenAlexW2089716974

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.