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长链非编码RNA LINC00673在糖尿病视网膜病变中表达下调，并通过负调控p53来调节视网膜色素上皮细胞的凋亡。

LncRNA LINC00673 is Downregulated in Diabetic Retinopathy and Regulates the Apoptosis of Retinal Pigment Epithelial Cells via Negatively Regulating p53.

作者信息

Cheng Yan, Zhu Yanxia, Ma Linli

机构信息

Department of Ophthalmology, The Second People's Hospital of Lianyungang, Lianyungang 222000, Jiangsu Province, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2021 Oct 13;14:4233-4240. doi: 10.2147/DMSO.S298185. eCollection 2021.

DOI:10.2147/DMSO.S298185
PMID:34675574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8520846/
Abstract

BACKGROUND

Long noncoding RNA (LncRNA) LINC00673 has been proven to play critical roles in cancer biology, while its role in other diseases is unknown. It has been reported that LINC00673 could interact with p53, a critical player in diabetes and diabetic complications, suggesting that LINC00673 may also participate in diabetic retinopathy (DR). This study aimed to investigate the role of LINC00673 in DR.

METHODS

The present study included 3 groups of participants, including DR group, diabetes (DB) group, and healthy control (Control) group. Flow cytometry was utilized to determine cell apoptosis. Proteins and messenger RNAs (mRNAs) were estimated by Western blot and quantitative reverse transcription PCR (qRT-PCR), respectively.

RESULTS

LINC00673 was downregulated in plasma samples of DR patients (n=60) in comparison with the healthy controls (n=60) and negatively correlated with p53 only across DR patients but not across the healthy controls. In retinal pigment epithelial cells (RPECs), high glucose treatment downregulated LINC00673. Moreover, LINC00673 overexpression downregulated p53 and decreased RPEC apoptosis, while LINC00673 silencing upregulated p53 and increased RPEC apoptosis. In addition, p53 overexpression reduced the effects of LINC00673 overexpression.

CONCLUSION

LINC00673 is downregulated in DR patients and regulates RPEC apoptosis via negatively regulating p53.

摘要

背景

长链非编码RNA（LncRNA）LINC00673已被证明在癌症生物学中起关键作用，而其在其他疾病中的作用尚不清楚。据报道，LINC00673可与p53相互作用，p53是糖尿病及糖尿病并发症中的关键因子，这表明LINC00673可能也参与糖尿病视网膜病变（DR）。本研究旨在探究LINC00673在DR中的作用。

方法

本研究纳入3组参与者，包括DR组、糖尿病（DB）组和健康对照组。采用流式细胞术检测细胞凋亡。分别通过蛋白质印迹法和定量逆转录聚合酶链反应（qRT-PCR）评估蛋白质和信使核糖核酸（mRNA）。

结果

与健康对照组（n = 60）相比，DR患者（n = 60）血浆样本中LINC00673表达下调，且仅在DR患者中LINC00673与p53呈负相关，而在健康对照组中无此相关性。在视网膜色素上皮细胞（RPECs）中，高糖处理可下调LINC00673。此外，LINC00673过表达可下调p53并减少RPEC凋亡，而LINC00673沉默则上调p53并增加RPEC凋亡。此外，p53过表达可减弱LINC00673过表达的作用。

结论

DR患者中LINC00673表达下调，并通过负向调节p53来调控RPEC凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/720fe863d81c/DMSO-14-4233-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/3a9a646c4ded/DMSO-14-4233-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/11f92fd67be7/DMSO-14-4233-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/d318250da158/DMSO-14-4233-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/720fe863d81c/DMSO-14-4233-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/3a9a646c4ded/DMSO-14-4233-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/11f92fd67be7/DMSO-14-4233-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/d318250da158/DMSO-14-4233-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c86/8520846/720fe863d81c/DMSO-14-4233-g0004.jpg

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