Objective: Glycation of LDL is significantly increased in diabetic patients. There is accumulating evidence that glycation of circulating lipoproteins, is implicated in the pathogenesis of diabetic atherosclerosis. Glycation, the nonenzymatic binding of glucose to protein molecules, can increase the atherogenic potential of certain plasma constituents, including low-density lipoprotein (LDL). In the present experiment, we investigated the proliferation of macrophage with glycated-LDL in the presence of several effectors such as M-CSF (Macrophage-Colony Stimulating Factor), PMA (Phorbol-12 Myristate 13-Acetate), LPS (Lipopolysaccharide) and dexamethasone.
Methods: Fresh LDL was glycated for 0, 10, 30, 60 and 180 days and differentiation of human monocyte derived
macrophage(HMDM) was tested. Also, glycated-LDL (50㎍/mL) with effectors such as M-CSF(15 ng/mL), PMA(120 ng/mL), LPS(10ng/ml) and dexamethason(1㎍/ml) were incubated on HMDM and compared differentiation with MTT assay.
Results: From the results, glycation of LDL increased differentiation of macrophage. And, M-CSF and PMA increased the differentiation of macrophage whereas LPS and dexamethason decreased.
Conclusion: It is thought that several effectors are involved in development of atherosclerosis, and we obtained the following conclusion that M-CSF and PMA might influence the development of atheroclerosis because they increased the viability of macrophage.