https://www.selleckchem.com/products/hs94.html Human hypertrophic scars are the result of imperfect healing of skin, which is particularly evident from the scars developing after severe burns. In contrast, mouse and rat full-thickness skin wounds heal normally without forming visible scar tissue, which reduces the suitability of rodent models for the study of skin scarring. We here provide a simple procedure to splint the edges of full-thickness rodent skin with a sutured plastic frame that prevents wound closure by granulation tissue contraction. The resulting mechanical tension in the wound bed and the lack of neo-epithelium amplify myofibroblast formation and generate hypertrophic features, not unlike those of human skin. In addition to producing scar tissue, the splint provides a reservoir that can be used for the delivery of cellular and acellular wound treatment regimen. Despite being simple and almost historical, wound splinting is a robust and reliable model to study myofibroblast biology.Mouse models are essential for investigation of underlying disease mechanisms that drive intestinal fibrosis, as well as assessment of potential therapeutic approaches to either prevent or resolve fibrosis. Here we describe several common mouse models of intestinal inflammation and fibrosis, including chemically driven colitis models, a bacterially triggered colitis model, and spontaneous intestinal inflammation in genetically susceptible mouse strains. Detailed protocols are provided for dextran sodium sulfate (DSS) colitis, 2,4,6-trinitro-benzene sulfonic acid (TNBS) colitis, adherent-invasive Escherichia coli (AIEC)-triggered colitis, the interleukin-10 knockout (IL-10KO) mouse model of spontaneous colitis, and the SAMP/YitFc model of spontaneous ileocolitis.Systemic sclerosis (SSc) is a rare systemic autoimmune disease associated with a high mortality. The first histopathological hallmarks are vasculopathy and inflammation, followed by fibrosis of the skin and internal