6JJ1 Oncostatin M (OSM), a member of the interleukin-6 (IL-6) cytokine family, acts on a variety of cells and elicits diversi®ed biological responses, suggesting potential roles in the regulation of cell survival, di erentiation and proliferation. 2 We have examined the e ect of OSM on the regulation of human lung ®broblast proliferation, collagen production and spontaneous apoptosis. The proliferative e ects of OSM (0.5 ± 100 ng ml 71 ) were assessed using a MTS assay as well as [ 3 H]-thymidine incorporation and cell counts at 24 and 48 h. Hydroxyproline was measured as an index of procollagen production by high pressure liquid chromotography (HPLC). Apoptosis was determined by annexin staining. 3 OSM enhanced the mitotic activity of lung ®broblasts in a time and dose dependent manner. Maximum proliferation of 57% above control was observed after incubation for 48 h with 2 ng ml 71 OSM (P50.05). 4 Incubation with the mitogen activated protein kinase (MAPK) kinase inhibitor, PD98059 or the tyrosine kinase inhibitor, genestein both signi®cantly reduced the mitogenic e ect of OSM (P50.05). 5 In contrast, proliferation in response to OSM was not regulated by induction of cyclo-oxygenase and subsequent prostaglandin E 2 (PGE 2 ) release or by IL-6. 6 OSM also stimulated ®broblasts to synthesize pro-collagen by a maximum of 35% above control levels after 48 h (P50.05). 7 OSM signi®cantly inhibited the spontaneous apoptosis of ®broblasts at 24 and 48 h. 8 These results provide evidence that OSM has pro-®brotic properties and suggest that it may play a role in normal lung wound repair and ®brosis.