Evidence map›Paper›PMID 31787761›Full record

ArticleCell death & disease2019

Rod bipolar cells dysfunction occurs before ganglion cells loss in excitotoxin-damaged mouse retina.

Yumeng Shen, Xue Luo, Shiliang Liu, Ying Shen, Scott Nawy, Yin Shen

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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  10. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
    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

6 authors at 4 institutions in 2 countries.

Yumeng ShenEye Center, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430060, Hubei Province, China.
Xue LuoEye Center, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430060, Hubei Province, China.
Shiliang LiuDepartment of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, Hubei Province, China.
Ying ShenMedical School, Zhejiang University, Hangzhou, 310053, Zhejiang Province, China.
Scott NawyDepartment of Molecular and Cell Biology, University of California Berkeley, Berkeley, 94720, CA, USA.
Yin ShenEye Center, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, 430060, Hubei Province, China. yinshen@whu.edu.cn.ORCID http://orcid.org/0000-0002-4201-3948
Zhejiang Chinese Medical University · CNTongji Hospital · CNUniversity of California, Berkeley · USWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive degeneration of retinal ganglion cells (RGCs) will cause a blinding disease. Most of the study is focusing on the RGCs itself. In this study, we demonstrate a decline of the presynaptic rod bipolar cells (RBCs) response precedes RGCs loss and a decrease of protein kinase Cα (PKCα) protein expression in RBCs dendrites, using whole-cell voltage-clamp, electroretinography (ERG) measurements, immunostaining and co-immunoprecipitation. We present evidence showing that N-methyl D-aspartate receptor subtype 2B (NR2B)/protein interacting with C kinase 1 (PICK1)-dependent degradation of PKCα protein in RBCs contributes to RBCs functional loss. Mechanistically, NR2B forms a complex with PKCα and PICK1 to promote the degradation of PKCα in a phosphorylation- and proteasome-dependent manner. Similar deficits in PKCα expression and response sensitivity were observed in acute ocular hypertension and optic never crush models. In conclusion, we find that three separate experimental models of neurodegeneration, often used to specifically target RGCs, disrupt RBCs function prior to the loss of RGCs. Our findings provide useful information for developing new diagnostic tools and treatments for retinal ganglion cells degeneration disease.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell Cycle ProteinsDendritesDisease Models, AnimalElectroretinographyGlaucomaHEK293 CellsHumansMaleMice, Inbred C57BLNerve DegenerationNeurotoxinsN-MethylaspartatePhosphorylationProteasome Endopeptidase ComplexCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell Cycle ProteinsNeurotoxinsN-MethylaspartateNR2B NMDA receptorPrkcabp protein, mouseProteasome Endopeptidase ComplexProtein Kinase C-alphaReceptors, N-Methyl-D-AspartateUbiquitin

Identifiers

PMID31787761
PMCPMC6885518
OpenAlexW2990476750

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.