Interferon-beta, an autocrine cytokine, suppresses human fetal skin fibroblast migration into a denuded area in a cell monolayer but is not involved in the age-related decline of cell migration.

The migration of human skin fibroblasts into a denuded area in a cell monolayer declined during in vitro and in vivo aging. We carried out a study to determine whether this age-related decline in cell migration was mediated by the autocrine cytokine interferon-beta (IFN-beta), which has been reported to suppress the proliferation, chemotaxis and collagen synthesis of human fibroblasts. Actually, IFN-beta specifically suppressed the migration of TIG-3S human fetal skin fibroblasts into a denuded area in a cell monolayer, as shown by the dose response experiments of IFN-beta and neutralizing anti-IFN-beta antibody. IFN-beta also inhibited their collagen synthesis but the addition of type I collagen could not reverse IFN-beta-induced inhibition of cell migration. Double strand RNA, which has been generally known to induce IFN-beta in human skin fibroblasts, suppressed the migration of TIG-3S cells. Next, a study was done to determine whether IFN-beta and double strand RNA suppressed the migration of TIG-3S cells in late passages as well as early passages, or whether neutralizing anti-IFN-beta antibody stimulated the migration of TIG-3S cells in late and middle passages. IFN-beta and double strand RNA suppressed the migration of TIG-3S cells in middle (PD45) and late (PD55) passages as well as in early passages (PD23-28). Neutralizing anti-IFN-beta antibodies could not reverse the low migratory activity of middle and late passage cells to the high migratory activity of early passage cells. These results indicated that the autocrine cytokine IFN-beta did not seem to be involved in the age-dependent decline of fibroblast migration.