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Updated: Jun 22, 2025
A Patient-Derived Xenograft Model for Venous Malformation
Published on: June 15, 2020
Gene expression profiling of venous malformations identifies the role of SDC1 in venous endothelial cells
1Henan Provincial People's Hospital, Henan Eye Hospital, Henan Eye Institute, People's Hospital of Zhengzhou University, Zhengzhou, China.
Objective:
To obtain insight into the molecular process implicated in venous malformations (VMs) and identify potential targets for treatment of VMs, this study profiled the gene expression pattern in VMs, investigated alterations of syndecan-1 (SDC1) expression in VMs, and tested the hypothesis that aberrant SDC1 expression triggers abnormal angiogenesis and VM development.
Methods:
Microarray analysis was performed to identify differentially expressed genes (DEGs) on a transcriptome-wide level in VMs and conjunctive normal. Gene Ontology molecular functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were carried out to establish enhancement of biological signaling pathways involved in VMs. Among the DEGs, we focused on SDC1, which is involved in matrix remodeling, cell proliferation and invasion, and angiogenesis. SDC1 expression in VMs was verified by qRT-PCR, western blotting, and immunohistochemistry. Loss-of-function of SDC1 was achieved in human umbilical vein endothelial cells (HUVECs) by siRNA to investigate the roles of SDC1 in cell migration, invasion, and angiogenesis.
Results:
Compared with control tissue, the transcriptome study identified 274 upregulated DEGs and 3 downregulated DEGs. The transcript and protein levels of SDC1 were significantly decreased in VMs compared with normal tissue. Inhibition of SDC1 enhanced HUVEC migration, invasion, and angiogenesis.
Conclusion:
Our genome-wide microarray analysis suggests the involvement of numerous genes in VMs. Among them, SDC1 plays a substantial role in the process of angiogenesis and development of VMs. SDC1 may represent a potential target for a molecular therapy for VMs.
Insights
Syndecan-1 (SDC1) is significantly decreased in venous malformations (VMs), and its inhibition promotes angiogenesis. This suggests SDC1 could be a therapeutic target for treating VMs.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Genomics
Background:
- Venous malformations (VMs) are complex vascular anomalies.
- Understanding the molecular mechanisms underlying VM development is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the gene expression patterns in VMs.
- To identify potential therapeutic targets for VMs.
- To explore the role of syndecan-1 (SDC1) in VM development and angiogenesis.
Main Methods:
- Genome-wide microarray analysis to identify differentially expressed genes (DEGs) in VMs.
- Gene Ontology and KEGG pathway analysis to understand biological signaling.
- Validation of SDC1 expression using qRT-PCR, western blotting, and immunohistochemistry.
- In vitro studies using human umbilical vein endothelial cells (HUVECs) to assess SDC1 function.
Main Results:
- Microarray analysis revealed 274 upregulated and 3 downregulated DEGs in VMs.
- SDC1 transcript and protein levels were significantly reduced in VMs compared to normal tissue.
- Inhibition of SDC1 in HUVECs led to enhanced cell migration, invasion, and angiogenesis.
Conclusions:
- SDC1 plays a significant role in angiogenesis and the development of VMs.
- Reduced SDC1 expression is a key feature of VMs.
- SDC1 represents a potential molecular target for VM therapy.
