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Intracellular Cholesteryl Ester Hydroperoxides And Hydroxides- Their Metabolism And Their Modulation Of Cell Function
Funder
National Health and Medical Research Council
Funding Amount
$182,029.00
Summary
Atherosclerosis is the disease which causes narrowings in arteries underlying such serious medical conditions as heart attack and stroke. A key component in the formation of atherosclerotic narrowings is the accumulation of fat-filled cells called foam cell macrophages in artery walls. Our study investigates the nature of the fats that macrophages accumulate, and how mild modification of these fats changes the metabolism of the macrophage. Cholesterol circulates in the blood stream as specialise ....Atherosclerosis is the disease which causes narrowings in arteries underlying such serious medical conditions as heart attack and stroke. A key component in the formation of atherosclerotic narrowings is the accumulation of fat-filled cells called foam cell macrophages in artery walls. Our study investigates the nature of the fats that macrophages accumulate, and how mild modification of these fats changes the metabolism of the macrophage. Cholesterol circulates in the blood stream as specialised particles called lipoproteins. The lipoprotein containing most of the cholesterol is low density lipoprotein (LDL), so-called bad cholesterol. LDL is the main source of fat that accumulates in the artery wall in atherosclerosis. When in the artery wall, it is taken up by macrophages which develop a foamy appearance. The accumulation of LDL fats within macrophages is greatly enhanced by the prior modification of LDL. The most well known of these modifications is oxidation- a chemical process of fat spoilage as occurs with rancid butter. Mild oxidation of LDL is well known to occur in human atherosclerosis. However, the ability of macrophages to accumulate the products of mild oxidation has never been established. We have recently discovered that the lipid products of mild oxidation of LDL can build up in macrophages. We achieved this by developing a new system of feeding oxidised LDL to macrophages. Surprisingly, not only could these lipid oxidation products be internalised by the cells, but they progressively accumulated over time, and caused major disturbances in the ability of macrophages to clear ordinary fats inside the cell. This means that mild oxidation of LDL can cause secondary damage inside the macrophage, which is far greater than had previously been realised. This project investigates precisely how the oxidised LDL is metabolised by macrophages and how it disturbs other cell functions.Read moreRead less
Myeloperoxidase-catalysed Damage To Arterial Extracellular Matrix And Its Consequences
Funder
National Health and Medical Research Council
Funding Amount
$384,750.00
Summary
A heme enzyme (myeloperoxidase) has been shown to be present in the lesions present in diseased human arteries, and it has been reported that this enzyme contributes to the development of arterial disease via its ability to catalyse the formation of highly reactive oxidants. Recent studies have shown that the level of this enzyme correlate strongly with the presence of coronary artery disease, and that this enzyme may play a role in plaque rupture, a leading cause of sudden coronary death. It ha ....A heme enzyme (myeloperoxidase) has been shown to be present in the lesions present in diseased human arteries, and it has been reported that this enzyme contributes to the development of arterial disease via its ability to catalyse the formation of highly reactive oxidants. Recent studies have shown that the level of this enzyme correlate strongly with the presence of coronary artery disease, and that this enzyme may play a role in plaque rupture, a leading cause of sudden coronary death. It has also been reported that elevated levels of metal ions are present in advanced human atherosclerotic lesions. In recent experiments we have shown that products generated by myeloperoxidase can interact with metal ions and superoxide radicals, and that this process results in an exacerbation of damage. This synergism between the oxidants generated by myeloperoxidase and metal ions may explain, at least in part, the complex mixture of products detected in human lesions and be responsible for the weakening of lesion structure and contribute to an enhanced likelihood of plaque rupture. This study will examine the potential effects and mechanisms of damage to extracellular matrix materials from normal arteries and cultured cells We will examine under what circumstances interactions occur and whether these reactions may play a key role in plaque rupture. We will also examine how materials arising from damage to the extracellular matrix may affect the cells whic grow upon this scaffolding, and whether this may be partly responsible for altered behaviour of cells within dveloping atherosclerotic lesions. A detailed knowledge of which processes are important in plaque rupture is an essential pre-requisite to the development of new therapeutic strategies.Read moreRead less