Journal
SCIENCE ADVANCES
Volume 7, Issue 34, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abg2712
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Funding
- Canadian Institutes of Health Research (CIHR)
- Heart and Stroke Foundation (HSF)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Canadian Foundation for Innovation (CFI)
- NSERC Vanier CGS-D scholarship
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The study identified a unique population of Gal3-expressing infiltrative macrophages in diabetic mice that play a crucial role in promoting vessel elimination after brain injury. Depletion of these infiltrative macrophages attenuated phagocytic activity and prevented the loss of blood vessels after injury.
The cellular events that dictate the repair of damaged vessels in the brain, especially in those with vascular risk factors such as diabetes, is poorly understood. Here, we dissected the role of resident microglia and infiltrative macrophages in determining the repair of ruptured cerebral microvessels. Using in vivo time-lapse imaging, gene expression analysis, and immunohistochemistry, we identified a unique population of phagocytic Galectin 3 (Gal3) expressing macrophages, distinct from resident microglia, which infiltrated and aggregated at the site of injury in diabetic mice and were associated with the elimination of microvessels. Depletion of these infiltrative macrophages in diabetic mice attenuated phagocytic activity and prevented the loss of blood vessels after injury. These findings highlight a previously unknown role for infiltrative Gal3 expressing macrophages in promoting vessel elimination after brain injury and provide impetus for future studies to determine whether depleting these cells can facilitate vascular repair in at risk populations.
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