Galectin 3 could play key role in vascular repair and loss in the diabetic brain after trauma

When stroke or other trauma damages the brain’s vascular system, immune cells rush to the site of injury. While we know these immune cells arise from both the brain (i.e., microglia) and the circulation system (i.e., macrophages), we don’t really understand how they moderate the repair of damaged vessels in the brain, especially in those with vascular risk factors like diabetes.

Dr. Eslam Mehina (Brown Lab, Division of Medical Sciences) helps fill in this knowledge-gap in her new first-author paper in Science Advances.

Using in vivo 2-photon microscopy and confocal imaging, Dr. Mehina and the other research team members identified a circulating population of hungry (i.e., phagocytic) immune cells that express a protein called Galectin 3. When these cells infiltrate and gather at an injury site in the diabetic brain, it usually leads to the loss of the damaged blood vessels instead of their repair. To rectify this problem, Dr. Mehina and the team discovered that chemically depleting the infiltrative immune cells in diabetic individuals reduced the abnormal phagocytic activity and prevented the loss of blood vessels after injury.

These findings highlight a novel role for Galectin 3—expressing macrophages in promoting vessel loss after injury. This data suggests the depleting these immune cells of Galectin 3 could be a viable therapy to facilitate vascular repair in at-risk populations and reduce vascular loss.

Dr. Mehina, who graduated from the UVic Neuroscience Graduate Program in 2021, notes there are many similarities between this new publication and her dissertation. “The publication includes much of the data from Chapters 3 and 4 of my dissertation and expands on it with additional findings from the other authors. They added qPCR data to look at changes in gene expression in the brain with diabetes or microbleeds, as well as additional confocal microscopy that further demonstrates colocalization of endothelial cells within Galectin 3—expressing macrophages,” she says.