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The role of CD55 in protecting the tumour environment from complement attack
J Morgan1, I Spendlove, L G Durrant
1The University of Nottingham, Cancer Research UK, Nottingham, UK.
Tissue Antigens
|November 26, 2002
Summary
Vascular endothelial growth factor (VEGF) increases cell surface CD55 and extracellular matrix deposition. Matrix metalloproteinase-7 (MMP-7) releases active CD55 from the extracellular matrix, suggesting a role in inflammation and invasion.
Area of Science:
- Immunology
- Cell Biology
- Oncology
Background:
- CD55 (also known as decay-accelerating factor) is a complement regulatory protein protecting cells from complement-mediated damage.
- Tumor cells overexpress CD55, depositing it into the tumor matrix.
- Tumor-derived VEGF upregulates endothelial CD55 and matrix metalloproteinases (MMPs).
Purpose of the Study:
- To investigate the effects of VEGF on CD55 deposition into the extracellular matrix (ECM).
- To determine the role of MMPs in releasing CD55 from the ECM.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) and a tumor cell line were treated with VEGF.
- CD55 expression and deposition in the ECM were analyzed.
- The release of CD55 from the ECM by various enzymes, including MMP-7, was assessed.
Main Results:
- VEGF upregulated CD55 on both cell surfaces and within the ECM.
- VEGF-induced CD55 release into the ECM by HUVECs was comparable to tumor cells with higher surface CD55 expression.
- MMP-7 released intact, functional CD55 from the ECM, unlike papain or collagenase.
Conclusions:
- VEGF promotes CD55 deposition in the ECM.
- MMP-7 plays a role in releasing functional CD55 from the ECM.
- CD55 released by MMP-7 may protect cells during inflammation and invasion.