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Atg16L1 作为糖尿病视网膜病变的新型生物标志物和自噬基因。

Atg16L1 as a Novel Biomarker and Autophagy Gene for Diabetic Retinopathy.

机构信息

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.

Department of Ophthalmology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.

出版信息

J Diabetes Res. 2021 Mar 18;2021:5398645. doi: 10.1155/2021/5398645. eCollection 2021.

DOI:10.1155/2021/5398645
PMID:33791389
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7997773/
Abstract

OBJECTIVE

Accumulating evidence suggests the critical role of autophagy in the pathogenesis of diabetic retinopathy (DR). In the current study, we aim to identify autophagy genes involved in DR via microarray analyses.

METHODS

Gene microarrays were performed to identify differentially expressed lncRNAs/mRNAs between normal and DR retinas. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of lncRNA-coexpressed mRNAs were used to determine the related pathological pathways and biological modules. Real-time polymerase chain reactions (PCR) were conducted to validate the microarray analyses.

RESULTS

A total of 2474 significantly dysregulated lncRNAs and 959 differentially expressed mRNAs were identified in the retina of DR. Based upon Signalnet analysis, Bcl2, Gabarapl2, Atg4c, and Atg16L1 participated the process of cell death in DR. Moreover, real-time PCR revealed significant upregulation of Atg16L1.

CONCLUSION

This study indicated the importance and potential role of Atg16L1, one of the autophagy genes, as a biomarker in DR development and progression.

摘要

目的

越来越多的证据表明自噬在糖尿病视网膜病变(DR)的发病机制中起着关键作用。在本研究中,我们旨在通过微阵列分析鉴定参与 DR 的自噬基因。

方法

进行基因微阵列分析,以鉴定正常和 DR 视网膜之间差异表达的 lncRNA/mRNA。lncRNA 共表达 mRNAs 的基因本体论和京都基因与基因组百科全书分析用于确定相关的病理途径和生物模块。实时聚合酶链反应(PCR)用于验证微阵列分析。

结果

在 DR 的视网膜中发现了总共 2474 个明显失调的 lncRNA 和 959 个差异表达的 mRNA。基于 Signalnet 分析,Bcl2、Gabarapl2、Atg4c 和 Atg16L1 参与了 DR 中的细胞死亡过程。此外,实时 PCR 显示 Atg16L1 显著上调。

结论

本研究表明自噬基因之一 Atg16L1 作为 DR 发展和进展的生物标志物的重要性和潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/a0d2b6347fe2/JDR2021-5398645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/003683896c4c/JDR2021-5398645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/7c73c42bb56a/JDR2021-5398645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/17443d8caa33/JDR2021-5398645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/a0d2b6347fe2/JDR2021-5398645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/003683896c4c/JDR2021-5398645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/7c73c42bb56a/JDR2021-5398645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/17443d8caa33/JDR2021-5398645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2712/7997773/a0d2b6347fe2/JDR2021-5398645.004.jpg

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