Evidence map›Paper›PMID 22511847›Full record

ArticleMolecular vision2012

High-mobility group box 1 protein is implicated in advanced glycation end products-induced vascular endothelial growth factor A production in the rat retinal ganglion cell line RGC-5.

Jong-Jer Lee, Chang-Chun Hsiao, I-Hui Yang, Ming-Huei Chou, Chia-Lin Wu, Yin-Chu Wei, Chih-Hsin Chen, Jiin-Haur Chuang

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Advanced glycation end products (AGEs) and their receptor (RAGE) induce apoptosis of periodontal ligament fibroblasts.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
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  20. Vitreous mediators in retinal hypoxic diseases.Mediators of inflammation · 2013
    Review
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

8 authors at 1 institution in 1 country.

Jong-Jer LeeDepartment of Ophthalmology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chang-Chun Hsiao
I-Hui Yang
Ming-Huei Chou
Chia-Lin Wu
Yin-Chu Wei
Chih-Hsin Chen
Jiin-Haur Chuang
Kaohsiung Chang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHigh-mobility group box 1 protein (HMGB1) has been reported to be a potent proangiogenic factor induced by inflammatory stress. In this study, we explore the role of HMGB1 in advanced glycation end products (AGEs)-induced vascular endothelial growth factor A (VEGF-A) production in rat retinal ganglion cell line 5 (RGC-5) cells.

methodsThe VEGF-A protein and mRNA levels in conditioned medium of RGC-5 cells incubated with AGE-modified BSA (AGE-BSA) were examined with real-time PCR and enzyme-linked immunosorbent assay (ELISA), and BSA-treated cells were used as controls. The expression of HMGB1, c-Jun N-terminal kinase (JNK), extracellular-signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (p38 MAPK) was assessed with immunofluorescence and western blot analysis. Reactive oxidative species (ROS) were detected with flow cytometry measurements of peroxide-dependent oxidation of 2'-7'-dichlorofluorescein-diacetate (DCFH-DA). N-Acetyl-L-cysteine (NAC), glycyrrhizin (GZ), and SP600125 were used to block ROS, HMGB1, and JNK, respectively.

resultsCompared with the BSA controls, the RGC-5 cells incubated with AGE-BSA showed a dose- and time-dependent increase in VEGF-A mRNA and VEGF-A protein secretion in the supernatant, with the highest levels achieved at 24 h. AGE-BSA stimulated a significant release of HMGB1 in the supernatant and a significant increase of intracellular ROS production at 3 h. NAC blocked HMGB1 production in a dose-dependent manner. Blocking with GZ, NAC, and JNK significantly suppressed AGE-induced VEGF-A production.

conclusionsHMGB1 is implicated in the production of VEGF-A in retinal ganglion cell line-5 (RGC-5). Blocking HMGB1, ROS, or the JNK pathway may attenuate VEGF-A production, suggesting HMGB1 and related signaling molecules play a role in diabetic retinopathy.

Indexed as

AcetylcysteineAnimalsAnthracenesCattleCell LineCulture Media, ConditionedDose-Response Relationship, DrugExtracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedGlycyrrhizic AcidHMGB1 ProteinMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesRatsReactive Oxygen SpeciesRetinal Ganglion CellsAcetylcysteineAnthracenesCulture Media, ConditionedExtracellular Signal-Regulated MAP KinasesGlycation End Products, AdvancedGlycyrrhizic AcidHbp1 protein, ratHMGB1 ProteinMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasespyrazolanthroneReactive Oxygen SpeciesRNA, MessengerSerum Albumin, BovineVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID22511847
PMCPMC3327441
OpenAlexW2165714324

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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.