Abstract: It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers.

Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.

Abstract: The present invention relates to methods and compositions that control, i.e., antagonize/inhibit or agonize/stimulate, de novo glucocorticoid production in the skin. Such methods and compositions can be used for the prevention and/or treatment of a variety of skin conditions, including inflammation, acute wounds, chronic non-healing wounds, keloid, fibrotic or hypertrophic scars, and epithelial-derived cancer.

Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.

Abstract: Compositions and methods for antagonizing miRNAs that are overexpressed in chronic, non-healing wounds, as compared to healthy tissue, are disclosed. The miRNA antagonists are oligonucleotides that hybridize to selected pre-miRNA or mature miRNAs and prevent the miRNAs from binding to and downregulating their target mRNAs. Methods of using the miRNA antagonists to treat inflammatory disorders, including to promote healing of chronic, non-healing wounds and acute wounds are provided.

Abstract: It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers.

Abstract: The present invention relates to methods for identifying tissue sites in a chronic wound that are suitable for debridement and whether debridement procedure has been successful using particular biological markers of the cells within the tissue sites of the chronic wounds.

Abstract: The present invention relates to methods and compositions that control, i.e., antagonize/inhibit or agonize/stimulate, de novo glucocorticoid production in the skin. Such methods and compositions can be used for the prevention and/or treatment of a variety of skin conditions, including inflammation, acute wounds, chronic non-healing wounds, keloid, fibrotic or hypertrophic scars, and epithelial-derived cancer.