Factors Involved in the Control of Fibroblast Proliferation by Glucocorticoids: A Review

IT IS well established that glucocorticoids exert catabolic effects on connective tissue and delay wound healing. They induce skin atrophy partly by decreasing the proliferative capacity of skin fibroblasts and the synthesis of the ground substance. Despite extensive investigations, the mechanisms of these in vivo steroid effects remain a matter of controversy, since the studies performed to elucidate the actions of adrenal steroids on the proliferation of various types of fibroblasts in vitro have led to contradictory results. Some authors have indeed described an inhibition of the proliferation of fibroblast cultures treated with glucocorticoids, whereas others have reported a stimulatory action of these drugs on cell division. In the present paper, we have attempted to present a comprehensive review of the data and thus provide an explanation for the differences observed among in vitro experiments. In fact, many of the reported discrepancies may be due, in part, to the use of different experimental models, of different experimental schedules and culture conditions, and to the various methods employed to monitor cell proliferation. Moreover, the complexity of the actions of glucocorticoids in vivo may be explained by the demonstration that, in addition to their metabolic effects on fibroblasts, glucocorticoids also indirectly affect fibroblast proliferation by controlling the syntheses or actions of various factors produced by other cell types.