In this study, using loss- and gain-of-function rodent fetal wound models, we identified that fibromodulin (Fm) is essential for fetal-type scarless wound healing.
Applying electric fields to artificial wounds in cell culture dishes and real wounds in rodent corneas, the team detected epithelial cells rushing towards the wound center; reversing the field caused the cells to change direction.
Wounded, wounded, wounded!
Here, we show that fibromodulin (FMOD), a 59-kD small leucine-rich proteoglycan critical for normal collagen fibrillogenesis, significantly reduces scar formation while simultaneously increasing scar strength in both adult rodent models and porcine wounds, which simulate human cutaneous scar repair.
Since porcine skin is significantly thinker than rodent skin, full-thickness wounds, down to the fascia, were created with a #15 surgical blade by excising a 1.5 cm×0.5 cm ellipse of skin with its long axis running perpendicular to the lines of minimal tension.
We previously observed an inverse correlation between Fmod and Tgfβ1 levels during fetal wound healing in rodents.
Biologically synthesized silver nanoparticles (Agnp) were further impregnated in GGAA for extended evaluations in punch wound models in rodents.
Opioids at physiologically relevant concentrations promote angiogenesis in vitro, and in breast cancer and wound healing in rodents (Gupta et al, 2002; Poonawala et al, 2005; Singleton et al, 2006).
We developed a wound model in immunodeficient rodent and treated it with engineered vascularized constructs from endothelial progenitors or early vascular cells-derived from human induced pluripotent stem cells (hiPSCs) reprogrammed either from healthy donor or type-1 diabetic patient.
However, wound closure in the rodent back models relies heavily on tissue contraction and to a lesser degree on the formation of new tissue [ 3].
