Fibromodulin Deficiency Alters Temporospatial Expression Patterns of Transforming Growth Factor-β Ligands and Receptors During Adult Mouse Skin Wound Healing

The study found that fibromodulin (FMOD) deficiency in mice leads to altered expression patterns of transforming growth factor-β (TGF-β) ligands and receptors during different stages of skin wound healing. FMOD-null mice showed increased inflammation and TGF-β receptor levels during the early inflammatory stage, which correlated with faster epithelial migration. However, in the proliferative stage, these mice had more robust expression of TGF-β3 and its receptors, resulting in delayed dermal cell migration and proliferation, postponed granulation tissue formation, and increased scar size. In the remodeling stage, FMOD-null mice had reduced expression of TGF-β ligands and receptors, contributing to decreased collagen synthesis and abnormal collagen architecture. The study concluded that FMOD is critical for coordinating the temporospatial distribution of TGF-β ligands and receptors, suggesting that FMOD modulates TGF-β bioactivity to promote proper wound healing. The study used immunohistochemical staining, quantitative real-time PCR, and in vitro migration assays with primary dermal fibroblasts, with sample sizes of 9 for dermal protein expression, 4 for total wound RNA expression, and 6 for each group in migration assays, indicating a statistically significant difference with a p-value <0.05.