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Updated: Apr 19, 2026
Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells
Published on: December 11, 2020
Identification of oxidative stress-induced gene expression profiles in cavernosal endothelial cells
Chao Hu1, Yin-Ying Dong2, Ye-Hao Dong1
1Department of Urology, Affiliated Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, P.R. China.
Abstract:
The aim of the present study was to explore the regulation status of genes in oxidative stress (OS)‑induced endothelial dysfunction and to elucidate the mechanism of action of OS‑associated genes, which induce cavernosal endothelial dysfunction in erectile dysfunction (ED). OS was established in purified cavernosal endothelial cells (CECs) using xanthine/xanthine oxidase and the differentially expressed OS‑associated genes were analyzed using gene microarrays. In addition, an ED rat model was established through bilateral internal iliac artery ligation with hyperlipidemia and was verified by an intracavernosal pressure test. The selected OS‑associated genes were validated in the CECs and ED rat model using reverse transcription‑quantitative polymerase chain reaction. Student's t‑test and one‑way analysis of variance were performed using SBC analysis system. Gene microarray analysis revealed that 13090 (31.92%) genes were expressed in the control group, whereas 12039 (29.35%) genes were expressed in the treated group. The cut‑off value for differential expression was set at 2.0 fold‑change and 2480 genes were found to be differentially expressed compared with the control group. Of these cells, 1454 were upregulated and 1026 were downregulated. Cluster analysis identified relevant cell signaling pathways that were hypothesized to be significant in OS‑associated endothelial dysfunction, including the cytokine‑cytokine receptor interactions, nitrogen metabolism, coagulation cascades and cell adherens. Cxcl12, Tgfbr1, Asns, Bdkrb1 and Cdh3 genes showed a corresponding variation in the CECs and ED rat model compared with the results of the gene microarray analysis. In conclusion, in the present study, the network of differentially expressed genes and OS‑associated signaling pathways identified using gene microarray analysis were validated in the CECs and ED rat model. The results indicated that OS may lead to endothelial dysfunction through certain cell signaling pathways, inducing ED. However, further functional verification is required in order to elucidate the underlying mechanisms of OS‑associated cell signaling pathways in ED.
Insights
Oxidative stress triggers endothelial dysfunction in erectile dysfunction (ED) by altering gene expression. This study identified key genes and pathways involved, offering insights into ED mechanisms.
Area of Science:
- Vascular Biology
- Molecular Biology
- Genomics
Background:
- Endothelial dysfunction is a key factor in erectile dysfunction (ED).
- Oxidative stress (OS) is implicated in the pathogenesis of endothelial dysfunction.
- The specific genes and pathways regulated by OS in cavernosal endothelial cells (CECs) leading to ED remain incompletely understood.
Purpose of the Study:
- To investigate gene regulation in OS-induced endothelial dysfunction.
- To elucidate the mechanism of action of OS-associated genes in cavernosal endothelial dysfunction and ED.
- To identify and validate differentially expressed genes and signaling pathways in an ED model.
Main Methods:
- Oxidative stress was induced in purified CECs using xanthine/xanthine oxidase.
- Gene expression profiling was performed using microarrays to identify differentially expressed genes.
- An ED rat model was established via bilateral internal iliac artery ligation with hyperlipidemia.
- Selected genes were validated in CECs and the rat model using RT-qPCR.
Main Results:
- Gene microarray analysis revealed 2480 differentially expressed genes (1454 upregulated, 1026 downregulated) in OS-treated CECs.
- Pathway analysis identified significant pathways including cytokine-cytokine receptor interactions, nitrogen metabolism, coagulation cascades, and cell adherens.
- Genes such as Cxcl12, Tgfbr1, Asns, Bdkrb1, and Cdh3 showed consistent variations in both CECs and the ED rat model.
Conclusions:
- The study identified a network of differentially expressed genes and OS-associated signaling pathways involved in endothelial dysfunction and ED.
- OS may induce ED through specific cell signaling pathways, highlighting potential therapeutic targets.
- Further functional studies are necessary to fully elucidate the underlying mechanisms of OS-associated signaling in ED.
