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Showed a series of experiments that miR – 33a and 33b – ABCA1 , a protein known to inhibit both the production of HDL and the transport of cholesterol from peripheral tissues important – including foam cells – secure in the liver for disposal. Particular variants and mutations in the ABCA1 gene is risk of heart risk of heart disease. HDL that treating cholesterol-laden mouse macrophages with antisense RNA strands that block miR-33 increased activity of ABCA1 and reduced cellular cholesterol levels. Injection of the same miR-33 antisense molecules in mice a high fat diet resulted in a significant increase of animals HDL levels, but had no effect on the levels of LDL, triglycerides and glucose. ‘Our finding that miR-33 acts in combination with its SREBP host to maintain cholesterol levels seem the first known instance of cooperative regulation of a physiological pathway by a microRNA and its host gene,’explains N r? ‘These studies have also provided the impetus to investigate whether this could novel cholesterol-lowering regulatory mechanism are a therapeutic target a therapeutic target for cardiovascular disease. ‘ – ‘These studies are particularly timely, since the development of drugs that the ”has been HDL – way challenge ‘good, adds Robert Gerszten, director of clinical and translational research, MGH Heart Center, a co-author of the Science paper.

Oral administration is delayed a CT scan and should be to patients with CT should be avoided with a suspected diagnosis of an acute appendicitis, he said. This study are on Tuesday are presented May at 17.40 clock Pacific Time.

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