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pmid:36686430

Autophagy and senescence of rat retinal precursor cells under high glucose.

Hanhan Peng · Wentao Han · Benteng Ma · Shirui Dai · Jianfeng Long · Shu Zhou · Haoyu Li · Baihua Chen

Frontiers in endocrinology · 2022 doi:10.3389/fendo.2022.1047642

Paper

complete

Experiment

complete

Data

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Analysis

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Execution

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title
Autophagy and senescence of rat retinal precursor cells under high glucose.
doi
10.3389/fendo.2022.1047642
pmid
36686430
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Hanhan Peng
[1]
Wentao Han
[2]
Benteng Ma
[3]
Shirui Dai
[4]
Jianfeng Long
[5]
Shu Zhou
[6]
Haoyu Li
[7]
Baihua Chen
journal
Frontiers in endocrinology
year
2022
abstract
Backgrounds: Diabetic retinopathy (DR) is a common diabetic ocular disease characterized by retinal ganglion cell (RGC) changes. An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which is a primary pathological feature of retinal neurodegeneration in DR. Accumulated studies confirmed autophagy and senescence play a vital role in DR; however, the underlying mechanisms need to be clarified. Methods: This study included the microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) to conduct the bioinformatics analysis. The R software was used to identify autophagy-related genes (ARGs) that were differentially expressed in fibrovascular membranes (FVMs) and normal retinas. Co-expression and tissue-specific expression were elicited for the filtered genes. The genes were then analyzed by ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Set Enrichment Analysis (GSEA). R28 cells were cultured with high glucose, detected by reverse transcription-quantitative (RT-qPCR) and stained by apoptosis kit. Results: In the retina, 31 differentially expressed ARGs (24 up-regulated genes) were discovered and enriched. The enrichment results revealed that differentially expressed ARGs were significantly enriched in autophagy, apoptosis, aging, and neural function. Four hub genes (i.e., TP53, CASP1, CCL2, and CASP1) were significantly up-regulated. Upregulation of cellular autophagy and apoptosis level was detected in the hyperglycemia model in vitro. Conclusions: Our results provide evidence for the autophagy and cellular senescence mechanisms involved in retinal hyperglycemia injury, and the protective function of autophagy is limited. Further study may favour understanding the disease progression and neuroprotection of DR.
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Autophagy and senescence of rat retinal precursor cells under high glucose.
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clarified. Methods: This study included the microarray expression profiling dataset GSE60436 from G
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ected by reverse transcription-quantitative (RT-qPCR) and stained by apoptosis kit. Results: In t
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Complete file
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An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which is a primary pathological feature of retinal neurodegeneration in DR. Accumulated studies confirmed autophagy and senescence play a vital role in DR; however, the underlying mechanisms need to be clarified.\nMethods: This study included the microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) to conduct the bioinformatics analysis. The R software was used to identify autophagy-related genes (ARGs) that were differentially expressed in fibrovascular membranes (FVMs) and normal retinas. Co-expression and tissue-specific expression were elicited for the filtered genes. The genes were then analyzed by ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Set Enrichment Analysis (GSEA). 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