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Alterations in human endothelial cell morphology, proliferation and function by a macrophage-derived factor
M Heffernan1, A Chance, E V Hess
1Department of Rheumatology, St. Vincent's Hospital, Dublin, Ireland.
Irish Journal of Medical Science
|August 1, 1994
Summary
Macrophages in peripheral blood mononuclear cells (PBMCs) release factors that cause endothelial cell (EC) elongation. This process alters EC proliferation and function, potentially involving TNF-alpha and IL-1.
Area of Science:
- Endothelial cell biology
- Immunology
- Cellular signaling
Background:
- Endothelial cell (EC) morphology changes during inflammation and lymphocyte traffic.
- In vitro studies show EC shape changes upon exposure to peripheral blood mononuclear cell (PBMC)-conditioned media (CM).
Purpose of the Study:
- Identify the cell type responsible for EC elongation factors.
- Investigate changes in EC proliferation and function during PBMC-induced elongation.
- Determine the specific PBMC-derived products causing EC elongation.
Main Methods:
- Quantitative image analysis of ECs.
- Separation of PBMCs into subpopulations (macrophages, B cells, T cells).
- Treatment of cultured ECs with conditioned media from PBMC subpopulations.
- Use of recombinant factors (TNF-alpha, IL-1).
Main Results:
- Macrophages (M phi) are the primary source of EC elongating factors.
- EC elongation is associated with decreased proliferation and increased prostacyclin production.
- TNF-alpha combined with IL-1 are identified as key factors inducing EC elongation.
Conclusions:
- Macrophage-derived factors significantly influence EC morphology.
- PBMC-induced EC elongation may represent a shift from proliferation to secretion.
- TNF-alpha and IL-1 are likely mediators of PBMC-induced EC elongation.