Research

Our work revealed that hyperglycemia causes an enrichment of miR-486-5p in exosomes produced by cultured macrophages and those isolated from the plasma of human diabetic subjects suffering from cardiometabolic inflammation and atherosclerosis. Ongoing studies examine miR-486-5p as a source of atherosclerosis acceleration in diabetes.

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 Our findings identified IL4-polarized macrophages (IL4-exo), commonly known as “M2-macrophages” as a source of anti-inflammatory exosomes. MicroRNA cargo present in IL4-exo were identified as a source of their protective signaling properties. The microRNA enriched in IL4-exo robustly increased mitochondrial respiration, oxidative phosphorylation and suppressed inflammatory signaling by communicating this cluster of microRNA to recipient cells that reprogrammed bioenergetic metabolism.

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Our more recent findings revealed a capacity for IL4-exo to improve mitochondrial function in white adipose tissue that improved insulin sensitivity and glucose tolerance in obese diabetic mice. Our findings support the use of IL4-exosomes as novel therapeutics to control cardiometabolic diseases.

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Our team has built on a rich legacy of ApoE-related research in lipoprotein metabolism and atherosclerosis. We now address the new idea that this protein plays an important role in modulating the immune-regulatory properties of macrophage-exosomes.

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