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Terminal complement proteins C5b-9 release basic fibroblast growth factor and platelet-derived growth factor from
L R Benzaquen1, A Nicholson-Weller, J A Halperin
1Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
The Journal of Experimental Medicine
|March 1, 1994
Summary
The terminal complement complex (C5b-9) triggers endothelial cells to release growth factors, promoting cell proliferation. This discovery reveals a new mechanism in proliferative vascular disorders.
Area of Science:
- Vascular Biology
- Immunology
- Cell Biology
Background:
- Endothelial cells and vascular smooth muscle cells interact significantly in blood vessel wall biology.
- Growth factors from endothelial cells regulate vascular smooth muscle cell proliferation, both normally and pathologically.
- Endothelial deposits of the complement membrane attack complex (MAC, C5b-9) are observed in pathological tissues with early cell proliferation, such as atherosclerosis.
Purpose of the Study:
- To investigate the role of terminal complement C5b-9 proteins in signaling focal cell proliferation.
- To determine if C5b-9 can elicit the release of growth factors from endothelial cells.
Main Methods:
- Exposure of bovine aortic and human umbilical vein endothelial cells to the MAC (C5b-9).
- Measurement of released growth factors, specifically basic fibroblast growth factor and platelet-derived growth factor.
- Assessment of the mitogenic activity of released factors on various cell types, including Swiss 3T3, vascular smooth muscle, and glomerular mesangial cells.
Main Results:
- Both bovine aortic and human umbilical vein endothelial cells released basic fibroblast growth factor and platelet-derived growth factor in response to the MAC.
- These released mitogens stimulated DNA synthesis in Swiss 3T3, vascular smooth muscle, and glomerular mesangial cells.
Conclusions:
- The terminal complement complex (MAC, C5b-9) induces endothelial cells to release mitogenic growth factors.
- Complement-induced release of mitogens from endothelial cells represents a novel pathogenic mechanism contributing to proliferative disorders.