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[具体物质]在年龄相关性白内障中的异常表达及其对细胞增殖、凋亡和基因表达变化的影响。 (注:原文中“Aberrant expression of ”后面缺少具体物质名称)

Aberrant expression of in age-related cataract and its effect on cell proliferation, apoptosis and gene expression changes.

作者信息

Zhu Dan, Li Peng, Wang Li, He Yuan, Zhang Hui-Zi

机构信息

Department of Optometry, Xi'an Medical University, Xi'an 710021, Shaanxi Province, China.

Department of Ophthalmology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an 710054, Shaanxi Province, China.

出版信息

Int J Ophthalmol. 2023 Mar 18;16(3):333-341. doi: 10.18240/ijo.2023.03.01. eCollection 2023.

DOI:10.18240/ijo.2023.03.01
PMID:36935791
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10009602/
Abstract

AIM

To evaluate the regulation of the aberrant expression of () in the development of age-related cataract (ARC).

METHODS

Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analysis were employed to evaluate the expression of in ARC patients and healthy controls. The proliferation, apoptosis, cell cycle and epithelial-mesenchymal transition (EMT) of human lens epithelial cell (HLE-B3) were further analyzed under the condition of gene silence. Alteration of gene expression at mRNA level after knockdown were also evaluated by qRT-PCR on HLE-B3 cells.

RESULTS

The aberrant expression of was identified a clinically associated with the ARC. Silencing of promoted the apoptosis and inhibited the proliferation of HLE-B3 by blocking the cell cycle. Moreover, gene silence didn't affect the cytoskeleton of HLE-B3 but down-regulated the (), (), () and () expression levels in HLE-B3 cells. Silencing the gene induced EMT of the HLE-B3 cells by promoting the () expression.

CONCLUSION

Silencing of induces S-phase arrest, also inhibits the proliferation and enhance HLE-B3 apoptosis and EMT, and down-regulates the expression of , , and . Thus, the expression alteration of may play a critical role in the pathogenesis of ARC.

摘要

目的

评估()异常表达在年龄相关性白内障(ARC)发生发展中的调控作用。

方法

采用定量逆转录聚合酶链反应(qRT-PCR)和蛋白质免疫印迹分析评估ARC患者及健康对照者中()的表达。在()基因沉默条件下,进一步分析人晶状体上皮细胞(HLE-B3)的增殖、凋亡、细胞周期及上皮-间质转化(EMT)。通过对HLE-B3细胞进行qRT-PCR,评估敲低()后mRNA水平上基因表达的变化。

结果

()的异常表达被确定与ARC临床相关。()沉默通过阻断细胞周期促进HLE-B3细胞凋亡并抑制其增殖。此外,()基因沉默不影响HLE-B3细胞的细胞骨架,但下调HLE-B3细胞中()、()、()和()的表达水平。沉默()基因通过促进()表达诱导HLE-B3细胞发生EMT。

结论

()沉默诱导S期阻滞,抑制HLE-B3细胞增殖,增强其凋亡及EMT,并下调()、()、()和()的表达。因此,()表达改变可能在ARC发病机制中起关键作用。