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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
Published on: June 15, 2019
C7 is expressed on endothelial cells as a trap for the assembling terminal complement complex and may exert
Fleur Bossi1, Lucia Rizzi, Roberta Bulla
1Department of Life Sciences, University of Trieste, Trieste, Italy.
Blood
|January 31, 2009
Summary
Researchers discovered membrane-bound C7 (mC7) on endothelial cells, which controls inflammation. This novel mC7 acts as a trap for complement components, preventing excessive inflammatory responses.
Area of Science:
- Immunology
- Cell Biology
- Complement System
Background:
- The complement system is crucial in innate immunity.
- Soluble complement components can trigger inflammation.
Purpose of the Study:
- To investigate the localization and function of C7 on endothelial cells.
- To understand the role of membrane-bound C7 in regulating complement-mediated inflammation.
Main Methods:
- Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)
- Western blot analysis
- Northern blot analysis
- Mass spectrometry
- Endothelial cell culture
Main Results:
- Identified membrane-associated C7 (mC7) on endothelial cells, indistinguishable from soluble C7.
- mC7 associates with vimentin on the cell surface.
- Membrane-bound terminal complement complex (mTCC) formed by mC7 did not induce endothelial cell activation (adhesion molecules, IL-8 secretion, albumin leakage).
- mTCC protected endothelial cells from the pro-inflammatory effects of soluble SC5b-9.
Conclusions:
- Novel localization of C7 as a membrane-bound molecule on endothelial cells.
- mC7 may act as a regulatory mechanism to control excessive inflammation.
- mC7 functions as a trap for late complement components, mitigating pro-inflammatory responses.
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