Presence of Diabetic Complications in Type 1 Diabetic Patients Correlates with Low Expression of Mononuclear Cell AGE-Receptor-1 and Elevated Serum AGE

摘要: Receptors for advanced glycation endproducts (AGE-R) mediate AGE turnover, but can also trigger inflammatory genes that promote diabetic tissue injury and complications (DC). High levels reduced AGE-R sites in kidneys of NOD mice prone to type 1 diabetes (T1D) renal disease (RD) suggested impaired function may contribute RD these mice. In this study, after confirming AGE-R1 expression mouse peritoneal macrophages, we tested differences AGE-R1, -R2, -R3 gene 54 human subjects by RT-PCR Western analysis. Fresh peripheral blood mononuclear cells (PBMN) were isolated from 36 persons: 18 T1D patients with severe (DC); 11 age-and DM-duration matched without DC (n-DC); 7 normal volunteers (NL). EBV-transformed lymphoblasts obtained an additional (12 patients, 6 DC, nondiabetics). mRNA protein PBMN n-DC enhanced (p n-DC) (n-DC AGE-R3, p <.05, <.05) compared NL. AGE-R2 correlated sAGE (r =.61, <.05), creatinine clearance = −.63, <.05). No noted cultured cells. The consistent pattern elevated serum low macrophages (NOD), fresh suggests ineffective regulation R1-mediated possibly genetic basis.