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Plasminogen activator inhibitor‐1 is elevated, but not essential, in the development of bleomycin‐induced murine scleroderma

Accumulative data have demonstrated that plasminogen activator inhibitor‐1 (PAI‐1) plays an important role in the extracellular matrix metabolism; however, the involvement of PAI‐1 in scleroderma has not been fully elucidated. In this study, we investigated the role of PAI‐1 in bleomycin‐induced murine scleroderma. 100 µg of bleomycin was injected subcutaneously to the back skin of C3H/HeJ mice on alternate day for 4 weeks. Histopathological findings revealed that PAI‐1 was positive in macrophage‐like cells and fibroblastic cells in the dermis, in parallel with the induction of dermal sclerosis. PAI‐1 mRNA expression in the whole skin was up‐regulated at 1 and 4 weeks. The production of active PAI‐1 protein in the lesional skin was significantly increased 3 and 4 weeks after bleomycin treatment. Next, we examined whether dermal sclerosis is induced by bleomycin in PAI‐1‐deficient (PAI‐1–/–) mice. 10 µg of bleomycin was subcutaneously injected to PAI‐1–/– and wild type (WT) mice 5 days per week for 4 weeks. Histological examination revealed that dermal sclerosis was similarly induced even in PAI‐1–/– as well as WT mice. Dermal thickness and collagen contents in the skin were significantly increased by bleomycin injection in both PAI‐1–/– and WT mice, and the rate of increase was similar. These data suggest that PAI‐1 plays an important role, possibly via TGF‐β pathway activation. However, the fact that PAI‐1 deficiency did not ameliorate skin sclerosis suggest that PAI‐1 is not the essential factor in the development of bleomycin‐induced scleroderma, and more complex biochemical effects other than PA/plasmin system are greatly suspected.