LPS-mediated upregulation of A20 protein expression is blunted in aortae of diabetic, as compared to non-diabetic mice.

<p>(A) WB of A20 in abdominal aortae of diabetic and non-diabetic atherosclerosis-prone C57BL/6 and atherosclerosis-resistant FVB/N mice, 8 h after LPS treatment. GAPDH and βactin were used to correct for loading and quantify relative A20 expression by densitometry, as reported below the WB. Data shown are representative of 3 (non-diabetic) and 4 (diabetic) mice per time-point and illustrate the loss of LPS-induced A20 protein in diabetic mice, regardless of strain. The cuts between samples reflect the fact that these samples, while on the same gel and same experiment, were not contiguous. (B) A20 mRNA levels analyzed by real-time PCR 3 to 8 h after LPS injection in mouse abdominal aortae (n = 5 non-diabetic and 7 diabetic mice in C57BL/6 and 3 non-diabetic and 4 diabetic mice in FVB/N). Data shown demonstrates that LPS increases A20 mRNA levels in aortae of diabetic and non-diabetic C57BL/6 and FVB/N, albeit at a greater levels in diabetic mice. Expression of 18S ribosomal RNA was used to normalize expression of A20 mRNA, and the results were presented as mean±SEM of mRNA. Each sample was measured in duplicate.