Martin Friedlander, M.D., Ph.D.

Martin Friedlander is a Professor in the Department of Molecular Medicine at the Scripps Research Institute. His laboratory has had a long-standing interest in basic mechanisms of ocular angiogenesis and the identification and development of angiostatic compounds as well as stem-cell based therapies for the treatment of neurovascular degenerative diseases of the eye. Newly emerging paradigms describe the existence of trophic “cross-talk” between local vascular networks and the tissues they supply helping to maintain a functional differentiated state in a variety of organ systems.  In fact, endothelial cells (ECs) are also known to provide trophic substances that greatly stimulate self-renewal and expand neural differentiation of neural stem cells.  Given such inter-dependency of vascular ECs and surrounding tissues, it may be possible to use one cell type to rescue the other in the face of severe stress such as hypoxia or genetically encoded cell-specific degenerations.  Such a therapeutic approach would obviate the need to employ destructive treatment modalities and would facilitate repair of damaged, and maintenance of normal, retinal tissue. They have demonstrated that adult bone marrow contains a population of endothelial, and other, progenitor cells that can target activated astrocytes, a hallmark of many ocular diseases, and participate in normal developmental angiogenesis in neonatal mice or injury-induced neovascularization in the adult. Intravitreal injection of these cells from mice and humans can completely prevent retinal vascular degeneration ordinarily observed in mouse models of retinal degeneration; this vascular rescue correlates with functional neuronal rescue as well. They have explored the potential clinical utility of these cells to treat retinal vascular and neurodegenerative diseases and, in addition, have used human induced pluripotent stem cells to differentiate populations of RPE cells that have a potent rescue effect in animal models of retinal neurovascular degenerative diseases. The molecular basis of these rescue effects has been investigated and they can substitute small molecules for intact cells under certain conditions.