A new study describes how a carbohydrate-binding protein, galectin-3, promotes angiogenesis, the growth of new blood vessels. Targeting the protein, scientists identified two approaches that significantly reduced angiogenesis in mice. These discoveries, published online August 16 in the Journal of Experimental Medicine, may lead to novel treatments for diseases caused by excessive angiogenesis, including age-related macular degeneration, a leading cause of vision loss in the elderly, as well as cancer, and diabetes.

When the body needs to expand its network of blood vessels, cells release molecular signals called growth factors that prompt angiogenesis. While this process is critical for normal growth, development, and wound healing, it can be harmful when blood vessels supply tumors or other diseased tissue, or when excessive blood vessel growth encroaches on surrounding tissues.

A growing body of research indicates that a protein called galectin-3 promotes angiogenesis, indicating that it may be a valuable target for drugs that halt harmful blood vessel growth. Until now, though, scientists did not understand how galectin-3 promotes angiogenesis.

Led by Noorjahan Panjwani, Ph.D., a professor in the department of ophthalmology at Tufts University School of Medicine, researchers propose a mechanism that explains how galectin-3 brings about angiogenesis. “Our study showed that galectin-3 protein binds to glycans (carbohydrate portions) of specific cell-adhesion proteins called integrins to activate the signaling pathways that bring about angiogenesis,” said Panjwani. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis.”

Dr. Panjwani’s team found that application of a galectin-3 inhibitor significantly reduced angiogenesis in mice. They also found that preventing galectin-3 from binding with the integrins reduced angiogenesis. Cancer drugs that target integrins are in clinical development.

“By deciphering the mechanism of galectin-3 action, we were able to establish more than one therapeutic target. The more we know about how this pathway works, the more options we have for potential treatments,” said Panjwani.

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