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Syndecan-1 is known to be a potential contributor to sub-clinical inflammation in diabetic nephropathy (DN). Loss of syndecan-1 from the surface of podocytes is thought to lead to cell dysfunction, which leads to the detachment of viable podocytes from the glomerulus, an early feature of DN. Although the mechanisms of constitutive syndecan-1 shedding have been addressed by several studies, the pathological mechanisms are less elucidated. The aim of this investigation is to consider the role of the O-glycosylating enzyme C2GNT in syndecan-1 shedding by podocytes. Conditionally immortalised human podocytes were used to study the effect of hyperglycaemia and C2GNT knock-down on syndecan-1 shedding by these cells. Hyperglycaemia induced C2GNT activity in podocytes results in increased O-glycosylation on the surface syndecan-1 in cells treated with high glucose compared to percentage of normal glucose (219.5±145.7 vs. 100%, P<0.05). This increase in O-glycosylation is associated with an increase in the shedding of the syndecan-1 ectodomain by podocytes treated with high glucose compared to percentage of normal glucose (118.2±7.1 vs. 100%, P<0.05). Moreover, podocytes manipulated for C2GNT knockdown show reduced syndecan-1 shedding when treated with high glucose compared to wild type cells treated with high glucose (89.97±11.95 vs. 118.2±7.17, P<0.05). Our findings suggest that the activity of o-glycosylating enzyme C2GNT is raised in podocytes under diabetic conditions. We demonstrate for the first time a novel mecha nism of pathological syndecan-1 shedding induced by C2GNT activity. This excess syndecan-1 shedding by podocytes can contribute to podocyte dysfunction

The novel link between inflammatory enzyme C2GNT and the shedding of syndecan-1 in podocyte dysfunction