Wound Healing in skin is a dynamic process that involves continuous sequences of signals and responses from cells like fibroblasts and keratinocytes. An imbalance in the signals and responses at the wound site may result in an over-healing process known as hypertrophic scar.
This scar, thick and fibrous, might inhibit movement when it results from serious burns over large areas, especially around a joint. In hypertrophic scars, the fibroblasts produce too much extracellular matrix (ECM) proteins – the “scaffolding” between cells – including collagen. They also produce too little matrix metaloproteinases (MMP), an enzyme involved in normal tissue breakdown and remodeling.
Keratinocytes are epidermal cells that release factors that will either prompt fibroblasts to produce MMP or keep them from producing collagen. Previous research has identified a factor called stratifin, which stimulates MMP production. However, the factors associated with the inhibition of collagen production have not yet been described.
Claudia Chavez-Munoz’s research seeks to identify and characterize the keratinocyte-derived factor(s) that may function as collagen inhibiting factors for dermal fibroblasts. Ultimately, she hopes that a better understanding of the factors involved in wound healing will lead to therapeutic strategies in order to improve or prevent hypertrophic scarring.