One of the nation's foremost vascular biologists, Dr. Timothy T. Hla, has been appointed as the new director of the Center for Vascular Biology and professor of pathology and laboratory medicine at Weill Cornell Medical College.

Founded in 1995, Weill Cornell's Center for Vascular Biology is dedicated to biomedical research into vascular disease -- specifically atherosclerosis and thrombosis -- and the contributing role of the vascular system in a wide range of diseases.

Previously leading the Center was its founding director, Dr. David P. Hajjar, executive vice provost and senior executive vice dean; dean of the Graduate School of Medical Sciences; and the Frank H.T. Rhodes Distinguished Professor of Cardiovascular Biology and Genetics and professor of biochemistry and pathology at Weill Cornell Medical College. After 15 years as director, Dr. Hajjar elected to step down in order to focus on comprehensive Medical College initiatives and responsibilities.

"Vascular biology is a tremendously fertile area for research. By better understanding the role of blood vessels in disease, we will improve our ability to develop new treatments for conditions from cancer to arthritis to heart disease," Dr. Hajjar says. "An accomplished researcher, administrator and teacher, Timothy Hla is uniquely qualified to lead this effort at Weill Cornell. Notably, he has made significant contributions to vascular biology across areas including the molecular basis of angiogenesis, the biology of the COX-2 pathway, sphingolipids as mediators in health and disease, and lipid mediators."

Dr. Hla's research into COX-2 has furthered scientific understanding of how this pathway is a molecular determinant of cancer progression and potentially a key component of the link between inflammation and cancer. He was the first to demonstrate exaggerated COX-2 expression in human chronic inflammatory disorders -- specifically rheumatoid arthritis. He subsequently discovered that COX-2 is over-expressed in human colorectal cancer tissues, and demonstrated that COX-2 over-expression in the mammary glands of transgenic mice results in invasive mammary cancer development.

As a postdoctoral fellow, Dr. Hla worked to clone mRNAs that arise during in vitro angiogenesis. During these efforts, he was able to clone the DNA for the orphan receptor EDG-1 (endothelial differentiation gene-1) -- the first-ever example of this kind of receptor in mammalian cell differentiation. And, in searching for EDG-1's binding site, he identified a platelet-derived lipid molecule called sphingosine-1-phosphate (S1P) -- a major discovery that brought together the fields of vascular biology and sphingolipid signaling. This research established S1P as an extracellular lipid mediator that acts in the extracellular environment to communicate between cells by binding to cell surface receptors. S1P receptor modulators are now in Phase III clinical trials to control inflammation in the treatment of multiple sclerosis.

Following the identification of the S1P receptor, Dr. Hla turned his attention to characterizing the signaling properties of S1P receptors and their actions on vascular cells, demonstrating the mechanisms behind formation of a stable vessel. He also showed that S1P signaling is important to tumor angiogenesis.

Dr. Hla's investigative studies have been well funded by the National Institutes of Health (NIH) and other granting agencies. Currently, Dr. Hla serves as principal investigator on two NIH-sponsored R01 awards. He was also granted a MERIT award from the NIH in 2006. In addition, his project grant was renewed by the NIH -- work that he will be continuing at Weill Cornell.

Dr. Hla has contributed significantly to a number of professional organizations and to the editorial boards of leading scientific journals. He has served on the council and as secretary-treasurer of the North American Vascular Biology Organization, and has served as a co-organizer of the 2003, 2005 and 2007 FASEB summer research conferences on lysophospholipids. He serves as editor-in-chief of the publications Prostaglandins and Other Lipid Mediators. He has also served as a member of the editorial boards of the Journal of Biological Chemistry, Vascular Pharmacology, The FASEB Journal, and Arthrosclerosis, Thrombosis and Vascular Biology.

Originally from Burma, Dr. Hla received his Ph.D. in biochemistry from George Washington University in 1988. Upon completion of a postdoctoral fellowship in the Laboratory of Molecular Biology at the American Red Cross, he was appointed Scientist I/assistant professor in the Department of Molecular Biology at George Washington University in 1991. He was promoted to Scientist II/associate professor in 1994. In 1996, Dr. Hla was recruited to the University of Connecticut School of Medicine, where he was appointed associate professor. Dr. Hla was appointed director of the Cell Biology Graduate Program in 1997, and director of the school's Center for Vascular Biology in 1998. He was promoted to professor of cell biology and of genetics and developmental biology in 2000.

"I very much look forward to collaborating with my new colleagues at Weill Cornell as we pursue a number of promising avenues for research," says Dr. Hla. "Specifically, we will be looking at the role of S1P signaling in regulating tumor development and the various ways by which COX-2 promotes cancer and angiogenesis. The longstanding strength in research areas of vascular biology, angiogenesis and hematology/oncology will allow us to branch into fruitful avenues in both basic and clinical research."

The Center for Vascular Biology

Under the direction of Dr. David P. Hajjar, the Center for Vascular Biology at Weill Cornell Medical College has made major contributions -- elucidating the biology of cells of the artery wall, the blood cells with which they interact, and the principal cellular and genetic changes that take place in arteries that predispose them to the formation of plaque and blood clots. Researchers at the Center have studied the interactions between blood cells and vessels, testing the hypothesis that mediators -- substances including nitrogen oxides, reactive oxygen species and growth factors -- regulate blood-vessel cell activity and plaque formation, and that atherosclerosis acts like a blood clot, forming a "response to injury."

Source
Weill Cornell Medical College

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