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Differential Effects of Human lnterleukin‐1 on Growth of Human Fibroblasts and Vascular Smooth Muscle Cells

Differential Effects of Human lnterleukin‐1 on Growth of Human Fibroblasts and Vascular... Monocyte products probably play a role in the initiation of smooth muscle cell proliferation in the arterial wall early in atherogenesis. Several groups have described mitogenic activity for arterial smooth muscle cells that is elaborated by mononuclear phagocytes (macrophage-derived growth factor). However, the biochemical nature of this mitogenic activity is unknown, lnterleukin-1 (IL-1) is a well-characterized monocyte product that activates the growth of mitogen-stimulated lymphocytes and promotes the growth of fibroblasts. We tested whether IL-1 also affects the growth of arterial smooth muscle cells and might account for some of the mitogenic activity produced by activated monocytes. Highly purified human IL-1 did stimulate the growth of human fibroblasts of either adult or fetal origin. However, under identical conditions, IL-1 lacked significant mitogenic effects on human, bovine, rabbit, or canine arterial smooth muscle cells. This mediator also failed to stimulate the growth of cultured human or bovine vascular endothelial cells, another cell type that may respond to macrophage-derived growth factor, lnterleukin-1 did not render smooth muscle cells competent to divide in the presence of plasma factors such as insulin (10−6M), or when growth of muscle cells was limited by incubation in a low (2%) concentration of serum. This monokine also failed to increase the mitogenic effect of purified platelet-derived growth factor on arterial smooth muscle cells incubated in serum-free medium. Thus, cultured human arterial smooth muscle cells differ from fibroblasts and lymphocytes in their response to human IL-1. Furthermore, since IL-1 lacks direct mitogenic effects on vascular smooth muscle cells, it does not account for the growth-promoting activity for smooth muscle cells that is elaborated by activated macrophages (macrophage-derived growth factor). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Differential Effects of Human lnterleukin‐1 on Growth of Human Fibroblasts and Vascular Smooth Muscle Cells

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Copyright
© 1985 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Monocyte products probably play a role in the initiation of smooth muscle cell proliferation in the arterial wall early in atherogenesis. Several groups have described mitogenic activity for arterial smooth muscle cells that is elaborated by mononuclear phagocytes (macrophage-derived growth factor). However, the biochemical nature of this mitogenic activity is unknown, lnterleukin-1 (IL-1) is a well-characterized monocyte product that activates the growth of mitogen-stimulated lymphocytes and promotes the growth of fibroblasts. We tested whether IL-1 also affects the growth of arterial smooth muscle cells and might account for some of the mitogenic activity produced by activated monocytes. Highly purified human IL-1 did stimulate the growth of human fibroblasts of either adult or fetal origin. However, under identical conditions, IL-1 lacked significant mitogenic effects on human, bovine, rabbit, or canine arterial smooth muscle cells. This mediator also failed to stimulate the growth of cultured human or bovine vascular endothelial cells, another cell type that may respond to macrophage-derived growth factor, lnterleukin-1 did not render smooth muscle cells competent to divide in the presence of plasma factors such as insulin (10−6M), or when growth of muscle cells was limited by incubation in a low (2%) concentration of serum. This monokine also failed to increase the mitogenic effect of purified platelet-derived growth factor on arterial smooth muscle cells incubated in serum-free medium. Thus, cultured human arterial smooth muscle cells differ from fibroblasts and lymphocytes in their response to human IL-1. Furthermore, since IL-1 lacks direct mitogenic effects on vascular smooth muscle cells, it does not account for the growth-promoting activity for smooth muscle cells that is elaborated by activated macrophages (macrophage-derived growth factor).

Journal

Arteriosclerosis – Wolters Kluwer Health

Published: Mar 1, 1985

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