Relationship And Mechanism Between Atherosclerosis And Calcification In Human Autopsy Carotid Artery Samples

Calcification of vessels was visualized as the outcome of passive degeneration involving a complex regulated process of bio-mineralization resembling osteogenesis.Proof shows that proteins controlling bone mineralization are involved in regulation of vascular calcification.Artery wall cells grown in culture prevail to become osteogenic by inflammatory and atherogenic incitement.In addition it has been shown that osteoclast-like cells are found in calcified atherosclerotic plaques and in active resorption of ectopic vascular calcification.Soft tissue calcification usually presents in areas of chronic inflammation,more or less working as a barrier limiting spread of the inflammatory stimulus.Atherosclerotic calcification is an example of such process,in which oxidized lipids are the inflammatory incitement.Calcification is used extensively as a clinical indicator of atherosclerosis.In atherosclerotic plaque,it is evident that calcification involves the participation of arterial osteoblasts and osteoclasts.The association between calcification and clinical events imparts to mechanical instability established by calcified plaque at its interface with softer non-calcified plaque.Usually as calcification continues,meeting surface area increases initially,but finally decreases as plaques merge.This occurrence may reckon for minimal calcification in unstable plaque.Calcification of vessels is worsened in certain clinical conditions including diabetes,menopause and osteoporosis.Mechanisms connecting them should be taken into account for clinical decisions.For example,osteoporosis treatments may have unpredictable effects on vascular calcification;the discoursealso applies.Additional understanding of processes controlling vascular calcification may produce new therapeutic options for vascular disease.Clinical expression of atherosclerosis is significantly influenced by plaque structure and composition.It is known that calcified atherosclerotic arteries may hold tissue that is histomorphologically indistinguishable from bone.Dystrophic mineral deposition and extracellular matrix calcification occurs in a lot of pathologic conditions through passive precipitation.Attention centered here on a specific type of mineral deposition with high significance to cardiac pathology: intimal arterial calcification in the perspective of atherosclerotic plaque.Through two dimensional electrophoresis(2DE)method and by mass spectrometry,(using proteins from atherosclerotic,calcified and normal of carotid artery samples),an investigation has been done to demonstrate that plaque calcification represents meeting of bone biology with chronic plaque inflammation.Protein similarity in atherosclerotic and calcified samples was compared to those from the normal sample.Some proteins have been found to be markedly upregulated(Thromboxane-A synthase,Titin,Tyrosine-protein kinase,Inositol 1,4,5-trisphosphate receptor type 2)and a downregulated protein(Alternative protein DCUN1D2)which has previously never been cited being linked to vascular calcification or atherosclerosis.This study confirms the expression of these proteins and their likely participation in atherosclerotic plaque formation and vascular calcification,with the detection of a novel gene for the first time in both atherosclerosis and calcification.Well-designed analysis of these specific proteins is indispensable to properly line up their part in atherosclerosis and calcification.It would then be possible to express whether their occurrence or absence is contributory of or is a compensatory retort to atherosclerotic calcification.