Diabetes mellitus impairs circulating proangiogenic granuloc
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Cardiovascular risk in diabetes is at least in part attributable to defective angiogenesis. Since diabetes negatively affects blood cells involved in angiogenesis, this study evaluated whether diabetes impairs proangiogenic granulocytes (PAGs).

The study characterised and quantified PAGs as CD49d+ granulocytes in peripheral blood of participants with type 2 or type 1 diabetes and in non-diabetic control participants. We evaluated PAG antigenic profile and assessed in vitro functional properties of CD49d+ granulocytes using 2D and 3D angiogenesis assays. Researchers also quantified PAGs before and after glucose control with a sodium-glucose cotransporter 2 (SGLT2) inhibitor, dapagliflozin. In parallel, we measured Ly6G+CD49d+ PAGs in streptozotocin-induced type 1-like diabetic mice vs non-diabetic control mice.

Results: PAGs were composed of eosinophils more than 80% and neutrophils more than 20%. Within both populations, CD49d identified CXCR4 high/VEGFR1 high cells. CD49d+ granulocytes supported in vitro angiogenesis by endothelial cells significantly more than CD49d− control granulocytes, and physically interacted with endothelial cells. Granulocytes type 2 diabetic participants had a profoundly impaired capacity to stimulate endothelial cell tubule formation compared with those non-diabetic control participants. CD49d+ PAGs were reduced by 30–40% and were functionally impaired in diabetic vs control individuals. PAG levels inversely correlated with plasma glucose and significantly increased 1.8-times after glucose control with dapagliflozin, which reduced HbA1c by 1.0%. Levels of Ly6G+CD49d+ PAGs were also significantly reduced also in type 1 diabetic mice vs control mice.

Conclusively, this study illustrates a significant impairment of PAGs in diabetes and provide evidence for a direct role of hyperglycemia. These findings add mechanistic information to explain the defective angiogenesis in diabetes.

Source: https://link.springer.com/article/10.1007/s00125-020-05142-3