Evidence map›Paper›PMID 26238997›Full record

ArticleBMC neuroscience2015

Receptor interacting protein 3-induced RGC-5 cell necroptosis following oxygen glucose deprivation.

Wei Ding, Lei Shang, Ju-Fang Huang, Na Li, Dan Chen, Li-Xiang Xue, Kun Xiong

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2015. 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
2.3field-weighted citation impact, top 12% 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, 40 citations in OpenAlex.

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  11. Changes of Necroptosis in Irbesartan Medicated Cardioprotection in Diabetic Rats.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Article
  12. Review
  13. Necroptosis in Hepatosteatotic Ischaemia-Reperfusion Injury.International journal of molecular sciences · 2020
    Review
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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

7 authors at 2 institutions in 1 country.

Wei DingDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. ldd2007200@163.com.
Lei ShangDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. shanglei1986@163.com.
Ju-Fang HuangDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. huangjufang@csu.edu.cn.
Na LiDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. 769049085@qq.com.
Dan ChenDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. 57460119@qq.com.
Li-Xiang XueDepartment of Biochemistry and Molecular Biology, Health Science Center, Peking University, Beijing, 100191, China. lixiangxue@hsc.pku.edu.cn.
Kun XiongDepartment of Anatomy and Neurobiology, Morphological Sciences Building, School of Basic Medical Sciences, Central South University, 172 Tongzi Po Road, Changsha, 410013, Hunan, China. xiongkun2001@163.com.
Central South University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNecroptosis is a type of regulated form of cell death that has been implicated in the pathogenesis of various diseases. Receptor-interacting protein 3 (RIP3), a member of the RIP family of proteins, has been reported as an important necroptotic pathway mediator in regulating a variety of human diseases, such as myocardial ischemia, inflammatory bowel disease, and ischemic brain injury. Our previous study showed that RIP3 was expressed in rat retinal ganglion cells (RGCs), where it was significantly upregulated during the early stage of acute high intraocular pressure. Furthermore, RIP3 expression was co-localized with propidium iodide (PI)-positive staining (necrotic cells). These results suggested that RIP3 up-regulation might be involved in the necrosis of injured RGCs. In this study, we aimed to reveal the possible involvement of RIP3 in oxygen glucose deprivation (OGD)-induced retinal ganglion cell-5 (RGC-5) necroptosis.

methodsRGC-5 cells were cultured in Dulbecco's-modified essential medium and necroptosis was induced by 8 h OGD. PI staining and flow cytometry were performed to detect RGC-5 necrosis. RIP3 expression was detected by western blot and flow cytometry was used to detect the effect of RIP3 on RGC-5 necroptosis following OGD in rip3 knockdown cells. Malondialdehyde (MDA) lipid peroxidation assay was performed to determine the degree of oxidative stress.

resultsPI staining showed that necrosis was present in the early stage of OGD-induced RGC-5 cell death. The presence of RGC-5 necroptosis after OGD was detected by flow cytometry using necrostatin-1, a necroptosis inhibitor. Western blot demonstrated that RIP3 up-regulation may be involved in RGC-5 necroptosis. Flow cytometry revealed that the number of OGD-induced necrotic RGC-5 cells was reduced after rip3 knockdown. Furthermore, MDA levels in the normal RGC-5 cells were much higher than in the rip3-knockdown cells after OGD.

conclusionsOur findings suggest that RGC-5 cell necroptosis following OGD is mediated by a RIP3-induced increase in oxidative stress.

Indexed as

AnimalsCell DeathCell HypoxiaCell LineGene Knockdown TechniquesGlucoseImidazolesIndolesLipid PeroxidationMalondialdehydeMiceOxidative StressReceptor-Interacting Protein Serine-Threonine KinasesRetinal Ganglion CellsUp-RegulationGlucoseImidazolesIndolesMalondialdehydenecrostatin-1Receptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouse

Identifiers

PMID26238997
PMCPMC4524047
OpenAlexW2105202196

What OpenQuestion holds

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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.