Evidence map›Paper›PMID 36562794›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Loss of pleckstrin homology domain and leucine-rich repeat protein phosphatase 2 has protective effects on high glucose-injured retinal ganglion cells via the effect on the Akt-GSK-3β-Nrf2 pathway.

Xuan Liu, Yong Liu, Li Chen, Zhichao Zhang, Lijun Cui, Ting Wei

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. The Healthy and Diseased Retina Seen through Neuron-Glia Interactions.International journal of molecular sciences · 2024
    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

6 authors at 2 institutions in 1 country.

Xuan LiuDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, China. liuxuan0831@xjtufh.edu.cn.
Yong LiuThe Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, No. 76 Yanta Road, Xi'an, 710061, Shaanxi, China. liuy5599@mail.xjtu.edu.cn.
Li ChenDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, China.
Zhichao ZhangThe Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, No. 76 Yanta Road, Xi'an, 710061, Shaanxi, China.
Lijun CuiDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, China.
Ting WeiDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, China.
First Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CN

Funding

Key Research & Development Program of Shaanxi Province No.2020SF-268Natural Science Basic Research Program of Shaanxi, China No.2020JM-400
6 · The paper itself

Abstract

objectivePleckstrin homology domain and leucine-rich repeat protein phosphatase 2 (PHLPP2) is linked to various pathological states. However, whether PHLPP2 mediates diabetic retinopathy is unaddressed. This work explored the biological function of PHLPP2 in modulating high glucose (HG)-elicited damage of retinal ganglion cells (RGCs), an in vitro model for studying diabetic retinopathy.

methodsMouse RGCs were treated with HG to establish a cell model. PHLPP2 was silenced by transfecting specific shRNAs targeting PHLPP2. RT-qPCR, immunoblotting, CCK-8 assay, flow cytometry, TUNEL assay, and ELISA were carried out.

resultsSignificant increases in PHLPP2 levels were observed in cultured RGCs exposed to HG. The severe damages evoked by HG to RGCs were remarkably weakened in PHLPP2-silenced RGCs, including improved cell survival, attenuated cell apoptosis, repressed oxidative stress, and prohibited proinflammatory response. The silencing of PHLPP2 strengthened the activation of Nrf2 in HG-treated RGCs via modulation of the Akt-GSK-3β axis. Interruption of the Akt-GSK-3β axis reversed PHLPP2-silencing-elicited Nrf2 activation. The protective effects of PHLPP2 silencing on HG-induced injury of RGCs were diminished by Nrf2 inhibition.

conclusionsThe loss of PHLPP2 was beneficial for HG-injured RGCs through the effect on the Akt-GSK-3β-Nrf2 pathway. This work suggests a possible role of PHLPP2 in diabetic retinopathy.

Indexed as

Diabetic RetinopathyProto-Oncogene Proteins c-aktAnimalsApoptosisGlucoseGlycogen Synthase Kinase 3 betaLeucine-Rich Repeat ProteinsMiceNF-E2-Related Factor 2Oxidative StressPleckstrin Homology DomainsProtein Phosphatase 2Retinal Ganglion CellsSignal TransductionGlucoseGlycogen Synthase Kinase 3 betaLeucine-Rich Repeat ProteinsNF-E2-Related Factor 2Protein Phosphatase 2Proto-Oncogene Proteins c-aktDiabetic retinopathyInflammationNrf2Oxidative stressPHLPP2Retinal ganglion cells

Identifiers

PMID36562794
OpenAlexW4312115081

What Socratic holds

Textmetadata
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 Socratic graph.