The role of the tumor suppressor gene NDRG2 in angiogenesis and wound healing

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The goal of the proposed research project is the development of cell-based therapy with activated dendritic cells and knockdown of the tumor suppressor gene N-myc downstream-regulated gene 2 (NDRG2) in a 2-year research fellowship at the Hagey Laboratory of the Division of Plastic and Reconstructive Surgery at Stanford University. The project aims at the characterization of novel therapeutic strategies for improvement of wound healing in malperfused extremities e.g. in patients with peripheral vascular disease (PVD) or diabetes mellitus. Regarding existing literature data and data from self-conducted research endeavors in the field of angiogenesis, NDRG2 appears to be promising target for novel and effective therapies to improve tissue perfusion. We hypothesize that dendritic cells cultivated from activated monocytes, which were pharmacologically stimulated (vitamin-D3 or dexamethasone) in order to down-regulate NDRG2, release pro-angiogenic cytokines and growth factors. After establishment of the cell-based strategy in several consecutive in vitro experiments for activation of endothelial cells, this technique will be used for induction of in vivo angiogenesis in a wound model in rats which has been developed by the group at the Hagey Laboratory at Stanford University. The final goal of this translational research approach will be a clinical application for the improvement of healing of chronic wounds.