Evidence map›Paper›PMID 25329584›Full record

ArticlePloS one2014

Potential role of Cyr61 induced degeneration of human Müller cells in diabetic retinopathy.

Fen Zhou, Yikui Zhang, Ding Chen, Zhitao Su, Ling Jin, Lei Wang, Zhixiang Hu, Zhisheng Ke, Zongming Song

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 90% 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

3 citing papers in PubMed, 10 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

9 authors at 3 institutions in 1 country.

Fen ZhouEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yikui ZhangEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Ding ChenEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhitao SuEye Center, Second Affiliated Hospital, College of Medicine, Zhejiang University, China.
Ling JinEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Lei WangEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhixiang HuEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhisheng KeEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zongming SongEye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Affiliated Eye Hospital of Wenzhou Medical College · CNSecond Affiliated Hospital of Zhejiang University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The degeneration of Müller cells has been recognized to involve in the pathogenesis of diabetic retinopathy. However, the mechanism is not yet clear. This study is to explore the potential role of Cyr61, a secreted signaling protein in extracellular matrix, in inducing human Müller cell degeneration in diabetic retinopathy (DR). Twenty patients with proliferative diabetic retinopathy (PDR) and twelve non-diabetic patients were recruited for this study. Vitreous fluid was collected during vitrectomy surgery for Cyr61 ELISA. Human Müller cell line MIO-M1 were cultured to be subconfluent, and then treated with glucose (0-20 mM) or Cyr61 (0-300 ng/ml). Cyr61 expression induced by increasing concentrations of glucose was evaluated by RT-qPCR and Western blot. Effects of Cyr61 on Müller cells viability, migration and apoptosis were observed by MTT assay, Transwell assay, and TUNEL assay. Vitreous Cyr61 levels were observed to be 8-fold higher in patients with PDR (3576.92 ± 1574.58 pg/mL), compared with non-diabetic controls (436.14 ± 130.69 pg/mL). Interestingly, the active PDR group was significantly higher than the quiescent PDR group (P<0.01). In retinal Müller cells culture, high glucose significantly and dose-dependently elevated Cyr61 expression at both mRNA and protein levels. Cyr61 at high concentrations dose-dependently inhibited the viability and migration of Müller cells. TUNEL assay further revealed that high concentration of Cyr61 significantly promoted the cell apoptosis. In conclusion, these findings demonstrated for the first time that the expression of Cyr61 was elevated by high glucose in Müller cells, and Cyr61 inhibited cell viability and migration while induced apoptosis, suggesting the potential role of Cyr61 in Müller cell degeneration. The elevated Cyr61 levels in vitreous fluid of PDR patients further support its role in diabetic retinopathy (DR).

Indexed as

AgedApoptosisCell LineCell MovementCell SurvivalCysteine-Rich Protein 61Diabetic RetinopathyEpendymoglial CellsFemaleGene Expression RegulationGlucoseHumansMaleMiddle AgedRNA, MessengerVitreous BodyCysteine-Rich Protein 61GlucoseRNA, Messenger

Identifiers

PMID25329584
PMCPMC4199605
OpenAlexW2082142291

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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.