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Dr. Riitta Taskinen
The understanding of the initiation of early atherosclerosis and vascular injury is critical for the prevention of atherosclerosis and also for targeted drug therapy. The role of inflammation and regulation of different transcription factors for the cholesterol update into macrophages as well as for the reverse cholesterol transport out of the cells are key steps.
Dr de Vries described novel transcription factors Nur77 that coexist with NR4A superfamily and expressed in both smooth muscle cells and macropgages. Interstingly, Nur77 in the vessel wall seems to be a protective factor because its expression protects against excessive proliferation of smooth muscle cells. This was shown in two different experimental models as well as using in vitro Nur77 activators. Nur 77 expression in macrophages was shown by both immunohistochemistry and in situ hybridization. Nur77 expression resulted in the inhibition of inflammatory genes in macrophages and reduced cytokine secretion as well as reduced lipid loading in these macrophages in vitro. Interestingly, Nur 77 seems to interact with lXRs in the vessel wall and this may be a key regulatory step. The role of Phospholipid transfer protein (PLTP) in atherosclerosis was debated but with no conclusion. Dr. Jauhiainen reported that PLTP exists in circualtion in two forms: active vs inactive. Active PLTP moderates phospholipid transfer from remnants into HDL particles and also participates in HDL remodelling. Interestingly, PLTP is also expressed in macrophages. PLTP knock out model was used to demonstrate the function of PLTP. In this KO model, mice the size of arterial lesions were markedly less than in wild type mice and the lipid profile was changed to anti- atherogenic direction with lower plasma triglcyeride and cholesterol together with increase of HDL. Thus macrophage PLTP deficiency influences clearly lipoprotein profile as well as atherosclerotic lesions. In conclusion active PLTP plays a role in the production of both pre beta HDL and large fused HDL particles that are acceptors for cholesterol efflux via ABCA1 and ABCG1 pathways respectively. Dr.Siegel reported an in vitro technique where the formation of nanoplaque surfaces were followed using incubation with LDL vs HDL. Ca ions were driving the process of LDL and HDL binding to heparinsulfate proteoglycans ( HS-PG). Interestingly HS-PG acted also as a flow sensor in vitro reflecting the endothelium – blood interface. Interestingly, LDL attenuated flow depedent dilation and increased vascular tension. Dr. Siegel also reported that flow-dependent relaxation was dependent on arterial plaque area. Furthermore, Fluvastatin therapy resulted in a marked reduction of nanoplaque formation and increased flow dilation.Finally, Dr Mezzetti discussed the factors regulating synthesis and breakdown of atheromatous plaques based on both animal models as well as in vitro experiments. The key observation was that simvastatin treatment for one month was able to reduce inflammatory infiltration in human arteries and stabilize different components in plaques. Thus starting therapy results in favourable modification of plaque biology.
Obviously we need new techniques to study macrophages and plaque biology. The identification of early steps in vascular injury will provide new tolls for targeted therapy to prevetnt atherosclerosis and vascular injury in the future.
New insights into atherosclerosis and vascular injury Symposium - The European Society of Cardiology and the European Atherosclerosis Society
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