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Alexander G. Marneros, MD, PhD

Assistant Professor, Department of Dermatology, Harvard Medical School

Assistant Professor, Dermatology, Massachusetts General Hospital

Contact Info

Alexander Marneros
Massachusetts General Hospital
149 13th Street
Charlestown, MA, 02129
Mailstop: CNY Rm 3.216
Phone: 617-643-7170
amarneros@partners.org

Assistant

Not Available.

DF/HCC Program Affiliation

Angiogenesis, Invasion and Metastasis

Research Abstract

I am a physician-scientist with an area of expertise in vascular biology, extracellular matrix biology and diseases associated with defects at basement membrane zones, such as various skin and ocular diseases. My interests stem from my training as a scientist, first as a graduate student and then as a post-doc in the laboratory of Dr. Bjorn R. Olsen at Harvard Medical School, but also from my clinical training during my residency in dermatology at New York Presbyterian Hospital of Columbia University.
Based on my experiences as a physician and a scientist, I am dedicated to pursue basic science as an independent investigator in the field of my expertise (about 80% effort) and provide teaching to medical students and residents, but also to provide patient care in dermatology (about 20% effort). The combination of clinical and scientific activities is aimed at translational research that provides novel bench-to-bedside approaches.

My research has focused on the molecular mechanisms that control blood vessel growth at basement membrane zones. I could demonstrate that genetic inactivation of the basement membrane component collagen XVIII/endostatin resulted in age-dependent basement membrane defects in the eye as seen in age-related macular degeneration in humans (Marneros et al., 2004 EMBO J.). This work provided the first mouse model for the “dry” form of age-related macular degeneration due to the lack of a basement membrane component. Furthermore, I could demonstrate that physiologic levels of a proteolytic fragment of collagen XVIII, endostatin, inhibits induced angiogenesis in vivo, and could for example reduce choroidal neovascularization (Marneros et al., 2007 FASEB J). The data suggest that blood vessel growth is regulated in part by pro- and anti-angiogenic factors derived from epithelial cells and from proteolytic degradation of the basement membrane. To provide further in vivo evidence for this hypothesis, I generated mice that lack the potent proangiogenic factor vascular endothelial growth factor (VEGF) specifically in epithelial tissues and examined the adjacent vasculature. Targeted inactivation of VEGF in the retinal pigment epithelium prevented the development of the choroidal vasculature, demonstrating the essential role of epithelium-derived VEGF for angiogenesis (Marneros et al., 2005, Am J Path). I am currently extending this work to study the role of pro- and anti-angiogenic factors for blood vessel functions and homeostasis in the adult in various tissues, including the skin and the eye. This work is supported by an independently funded NIH R01 grant.

My work as a physician and a scientist has provided me with the expertise and the means to engage in translational research aiming at answering important questions that arise from clinical observations to ultimately improve patient care.

Publications

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