Genetic and Biological Effects of ICAM-1 E469K Polymorphism in Diabetic Kidney Disease

Figure 3

Possible cellular mechanism of ICAM1 in the development of diabetic kidney disease. This schematic diagram implicates that ICAM1 DNA transcription in the nuclei and mRNA translation in plasma of endothelium cells is increased under a diabetic condition with hyperglycemia. Subsequently, the ICAM-1 protein expression on the surface of endothelium cells is upregulated. ICAM-1 protein binding activity with leukocyte adhesion protein-1 (LEA-1), which is from blood, is increased, while heterozygous of ICAM-1 E469K protein likely more actively binds with LFA-1. Thereby, more and more lymphocytes from blood due to combining ICAM-1 and IFA-1 are transferred through endothelium cells in glomeruli and peritubular capillaries of the nephron in the kidney. Consequently, injure of kidney glomeruli and tubular has occurred.