We are interested in developing angiogenesis-based approaches to treating type 2-diabetes, both by testing possible strategies in diabetic mice and through better understanding of fundamental aspects of blood vessel formation.

Project 1. Repair of injured vasculature in diabetic and non-diabetic mice. Type 2 diabetes has reached endemic levels, and leads to serious consequences such as heart attack, renal failure, blindness, amputation, and death. In spite decades of research, an effective treatment is still lacking. An important contributing factor to the devastating consequences of diabetes is loss and/or dysfunction of blood vessels in multiple tissues and organs. Destruction of blood vessels is not only a consequence of diabetic conditions, but also exacerbates the progression of diabetes because poor blood supply to multiple organs leads to further metabolic imbalance and therefore worsening of the disease. Thus, repair of diabetes-damaged blood vascular system treats both the symptom and cause.

Project 2. When blood vessels first form, they generally exist in a honeycomb pattern consisting of uniformly sized microvessels. To assume proper physiological functions, newly formed microvessels undergo extensive reorganization to form a tree-like hierarchical structure with clear distinctions of large trunks and progressively smaller branches. Very little is known about how this process is regulated, but yet such knowledge may be critical to the success of angiogenesis therapy. We are using the mouse retina as a model system to investigate the molecular and cellular mechanisms underlying this process.

Main technologies employed: manipulation of human induced pluripotent stem cells, genetic modification of mice, lentiviral vector-mediated overexpression and knockdown in mice, standard and live confocal imaging, microvascular surgery, laser Doppler imaging, conventional molecular biology and biochemistry, cell culture, and immunohistochemistry.

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