摘要
Excessive production of collagen is the hallmark of fatal diseases of fibrosis such as systemic sclerosis. Overexpression of the proteoglycan fibromodulin (FMOD) has been associated with improved wound healing and scarless repair. In this study, we have investigated the consequences of FMOD deficiency on the development of experimental skin fibrosis. Using immunohistochemistry, we identified FMOD in both human and murine fibrotic skin. In the bleomycin modelof skin fibrosis, FMOD-/- mice developed skin fibrosisto a similar degree compared to FMOD+/+ mice. Analysis of skin ultrastructure using transmission electron microscopy revealed a significant reduction in collagen fibrildiameter in FMOD-/- but not FMOD+/+ mice followingfibrosis. We conclude that the impact of FMOD deficiency on the development of experimental skin fibrosis is limited.
- 出版日期2016-7