Glycated albumin (Amadori product) induces activation of MAP kinases in monocyte-like MonoMac 6 cells

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Increased levels of glycated, Amadori-modified albumin are a risk factor for diabetic vascular disorders. Glycated albumin binds to specific receptors and induces cellular signaling pathways, the complexity of which is largely unknown. Binding of glycated albumin to MonoMac 6 cells leads to an activation of MAPK p44/42 (ERK1/2) and p38 with subsequent translocation of NF-κB into the nucleus. The activation of MAPK is in part mediated by protein kinase C activation, but a PKC-independent pathway via MEK-1 is also involved. Protein tyrosine kinases do not play a role in the activation of NF-κB. The results may have pathophysiological significance, because the MonoMac 6 cell line is not greatly different from blood monocytes.