Previous research had shown that galectin-3 was a novel proangiogenic molecule, but the mechanism by which galectin-3 promoted angiogenesis was unknown. Now, investigators at the Tufts University School of Medicine (Boston, MA, USA) have used a series of biochemical and genomic tools to establish how galectin-3 influences the process of angiogenesis.

They reported in the August 16, 2010, online edition of the Journal of Experimental Medicine that galectin-3 inhibitors as well as antibodies against the galectin-3 binding protein integrin alpha-v-beta-3 blocked angiogenesis in a mouse model. Similarly, angiogenesis was inhibited in mice genetically engineered to lack the galectin-3 gene. Stimulation of angiogenesis by galectin-3 was ultimately linked to its effect on the endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)-mediated molecular pathway.

"Our study shows that galectin-3 protein binds to glycans (carbohydrate portions) of specific cell-adhesion proteins, the integrins, to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis,” said senior author Dr. Noorjahan Panjwani, professor of ophthalmology at Tufts University Medical School. "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.”


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