Activated Glycogen Synthase Kinase-3β’s Ability to Inhibit Keloid Formation

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Keloid scars are abnormal wound healing processes characterized by excessive collagen deposition that exceed the borders of the original wound. Inactivated glycogen synthase kinase 3-β (GSK-3β), a molecule that breaks down β-catenin which is used by the Wnt/β-catenin pathway in hypertrophic scarring, has been found to be abundant in keloid fibroblasts. The Wnt/β-catenin pathway is known to influence hypertrophic scarring, and the activation of GSK-3β has been found to inhibit other hypertrophic scarring diseases. This project focuses on determining if activating GSK-3β will inhibit keloid formation by decreasing the collagen, elastin, and fibronectin levels. Human keloid fibroblasts were cultured in vitro and treated with sodium nitroprusside to activate GSK-3β, lithium chloride to inhibit GSK-3β, and a negative control. Protein levels were then assessed through Western Blot analysis. The results of this study suggest that GSK-3β is partially inactive in keloid fibroblasts and that activation of the protein activates the Wnt signaling pathway and decreases collagen and elastin production. Fibronectin levels were found to increase with treatment, but this may be explained by its role in cell adhesion and contraction in wound healing. Further research is needed to fully identify activated GSK-3β as a therapeutic target for keloid scar patients and individuals who are prone to keloid scarring.



Keloid, Glycogen synthase kinase 3-β, Wnt/β-catenin pathway, Wound healing