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Profile image of David Goukassian

    David Goukassian, MD, PhD

    Education

    MD, Yerevan Medical University

    PhD, Central Advanced Training Institute for Physicians

    Post-Doctoral Fellow, Boston University School of Medicine

    Post-Doctoral, Tufts University School of Medicine

    Research

    Since 1998, the focus of Dr. Goukassian's research efforts has been on identifying the role of TNF in ischemia-induced inflammation, tissue regeneration, therapeutic angiogenesis and gene therapy. My research is aimed at development of treatments based on TNF-TNFR1/p55 and -TNFR2/p75 ligand-receptor interaction, specifically, (1) development of therapies to improve post-ischemic repair, regeneration and neovascularization processes; (2) development of universal platform therapeutics to improve stem cell and gene therapy outcomes in damaged tissues. TNF, a pro-inflammatory cytokine, is highly expressed in any damaged tissue, and plays a key role in the repair and regeneration processes via its two receptors, TNFR1 (p55) and TNFR2 (p75), whereby p55 mediates cytotoxic effects while p75 is pro-survival. Inflammation is an important phase of tissue regeneration processes. Perturbations in the spatial distribution of inflammatory cells, changes in the type and magnitude of the inflammatory infiltrate, disrupted temporal sequence, results in a persistent rather than resolved inflammatory phase and functional impairment of the damaged tissue. As a pro-inflammatory cytokine, TNF induces apoptosis and blocks stem and progenitor cell differentiation. The key finding of my research in this field with major therapeutic implications is that - restoration or overexpression of TNFR2/p75 (gene therapy) or inhibition of TNFR2/p55 (neutralizing antibody or small molecules) improves recovery in damaged tissue through inhibition of prolonged inflammation and cell death, promotion of therapeutic angiogenesis and development of new vascular network, thereby creating tissue environment for recruitment, incorporation and function of endogenous and exogenous stem cells and increasing survival of the resident differentiated cells and adult stem cells. This approach will improve stem and progenitor cell-therapy effectiveness and outcomes and could serve as a universal platform for stem cell and gene therapy.