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周期蛋白依赖性激酶 1 被证明是化学性膀胱炎的潜在遗传靶点。

Cyclin-dependent kinase 1 shows to be a potential genetic target for chemical cystitis.

机构信息

Department of Surgical Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.

Department of Neurology, Suzhou Ninth People's Hospital, Suzhou, Jiangsu, China.

出版信息

Immun Inflamm Dis. 2021 Sep;9(3):950-958. doi: 10.1002/iid3.454. Epub 2021 Jun 3.

DOI:10.1002/iid3.454
PMID:34080795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8342199/
Abstract

BACKGROUND

In the present study, we aimed to explore whether common genetic targets or signaling pathways existed in chemical cystitis.

METHODS

Gene Expression Omnibus (GEO) database was used to search the related gene expression profiles. The differentially expressed genes (DEGs) were identified by using GEO2R. The DAVID 6.8 Beta and R software were used to perform Kyoto Encyclopedia of Genes and Genomes pathway analysis and Gene Ontology function analysis of DEGs. The protein-protein interaction network was constructed by STRING 11.0 to reveal the potential gene interactions. The expression of cyclin-dependent kinase 1 (Cdk1) at the messnger RNA (mRNA) and protein levels was examined by real-time polymerase chain reaction (PCR) and Western blot analysis analysis, respectively.

RESULTS

The GEO database was searched, and the gene expression profiles of GSE55986 and GSE68539 were downloaded. A total of 262 DEGs and 356 DEGs were identified from GSE55986 and GSE68539, respectively. We found that the p53 signaling pathway might play a key role in the development of chemical cystitis, and Cdk1 acted as a crucial gene in the p53 signaling pathway. Moreover, the experimental results of real-time PCR and Western blot analysis analysis demonstrated that the expression of Cdk1 at the mRNA and protein levels in cystitis tissues was significantly increased in different animal models of chemical cystitis compared with the control group.

CONCLUSION

Cdk1 might be a potential pathogenic genetic target for chemical cystitis.

摘要

背景

本研究旨在探讨化学性膀胱炎是否存在共同的遗传靶点或信号通路。

方法

使用基因表达综合数据库(GEO)搜索相关基因表达谱。使用 GEO2R 鉴定差异表达基因(DEGs)。使用 DAVID 6.8 Beta 和 R 软件对 DEGs 进行京都基因与基因组百科全书(KEGG)通路分析和基因本体论(GO)功能分析。通过 STRING 11.0 构建蛋白质-蛋白质相互作用网络,揭示潜在的基因相互作用。通过实时聚合酶链反应(PCR)和 Western blot 分析分别检测细胞周期蛋白依赖性激酶 1(Cdk1)在信使 RNA(mRNA)和蛋白质水平的表达。

结果

从 GEO 数据库中搜索并下载 GSE55986 和 GSE68539 的基因表达谱。从 GSE55986 和 GSE68539 中分别鉴定出 262 个 DEGs 和 356 个 DEGs。我们发现 p53 信号通路可能在化学性膀胱炎的发生发展中起关键作用,Cdk1 作为 p53 信号通路中的关键基因。此外,实时 PCR 和 Western blot 分析实验结果表明,与对照组相比,不同化学性膀胱炎动物模型的膀胱炎组织中 Cdk1 的 mRNA 和蛋白质水平表达均显著增加。

结论

Cdk1 可能是化学性膀胱炎的潜在致病遗传靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/6d53b4716534/IID3-9-950-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/4263d5b8d312/IID3-9-950-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/ff4209303f8f/IID3-9-950-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/6bf5ec98964b/IID3-9-950-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/5929432c8d90/IID3-9-950-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/6d53b4716534/IID3-9-950-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/4263d5b8d312/IID3-9-950-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/ff4209303f8f/IID3-9-950-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/6bf5ec98964b/IID3-9-950-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/5929432c8d90/IID3-9-950-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9612/8342199/6d53b4716534/IID3-9-950-g001.jpg

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