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

Author(s): Kirti Kaul | Mohit Chopra | Pamela De Angelis | Eva M. Kohner | Rakesh Chibber

Journal: Endocrinology Studies
ISSN 2038-9515

Volume: 2;
Issue: 2;
Start page: e9;
Date: 2012;
Original page

Keywords: core 2 β-1 | 6-N-acetylglucosaminyltransferase | syndecan-1 | oxidative stress | o-glycosylation | diabetes | diabetic nephropathy | inflammation

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
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