Tumor necrosis factor-α processing inhibitor-1 inhibits skin fibrosis in a bleomycin-induced murine model of scleroderma
作者： Mika Terao , Hiroyuki Murota , Shun Kitaba , Ichiro Katayama
DOI: 10.1111/J.1600-0625.2009.00973.X
关键词:
摘要: Elevated serum concentration of soluble tumor necrosis factor receptor p55 (sTNFRp55) is known to correlate with the severity systemic sclerosis (SSc). However, it has not been verified whether this increase contributes pathogenesis SSc. In study, we found that sTNFRp55 also increased in bleomycin (BLM)-induced murine model Therefore, examined effect factor-alpha processing inhibitor-1 (TAPI-1), inhibitor TNFRp55 sheddase, model. TAPI-1 was administered weekly mice skin fibrosis induced by daily BLM injections. significantly suppressed BLM-induced thickness and number myofibroblasts. It inhibited after 3 weeks The mRNA expression collagen type I alpha1, transforming growth factor-beta1 alpha smooth muscle actin were decreased administration. Taken together, these findings indicate targeting TNFalpha converting enzyme might be a new therapy for patients
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