Cholesterol ester hydrolase neutral

A few enzymes, such as the previously mentioned CNP, are believed to be fairly specific for myelin/oligodendro-cytes. There is much more in the CNS than in peripheral nerve, suggesting some function more specialized to the CNS. In addition, a unique pH 7.2 cholesterol ester hydrolase is also enriched in myelin. On the other hand, there are many enzymes that are not myelin-specific but appear to be intrinsic to myelin and not contaminants. These include cAMP-stimulated kinase, calcium/calmodulin-dependent kinase, protein kinase C, a neutral protease activity and phosphoprotein phosphatases. The protein kinase C and phosphatase activities are presumed to be responsible for the rapid turnover of MBP phosphate groups, and the PLP acylation enzyme activity is also intrinsic to myelin. 

Reproductive effects of molinate may depend on inhibition of neutral cholesterol ester hydrolase, leading to disruption of mobilization of cholesterol from high-density lipoprotein, a process selective for... 

The overall metabolism of vitamin A in the body is regulated by esterases. Dietary retinyl esters are hydrolyzed enzymatically in the intestinal lumen, and free retinol enters the enterocyte, where it is re-esterified. The resulting esters are then packed into chylomicrons delivered via the lymphatic system to the liver, where they are again hydrolyzed and re-esterified for storage. Prior to mobilization from the liver, the retinyl esters are hydrolyzed, and free retinol is complexed with the retinol-binding protein for secretion from the liver [101]. Different esterases are involved in this sequence. Hydrolysis of dietary retinyl esters in the lumen is catalyzed by pancreatic sterol esterase (steryl-ester acylhydrolase, cholesterol esterase, EC 3.1.1.13) [102], A bile salt independent retinyl-palmitate esterase (EC 3.1.1.21) located in the liver cell plasma hydrolyzes retinyl esters delivered to the liver by chylomicrons. Another neutral retinyl ester hydrolase has been found in the nuclear and cytosolic fractions of liver homogenates. This enzyme is stimulated by bile salts and has properties nearly identical to those observed for... 

Modified LDL taken up by the cell are delivered to the endolysosome pathway, where enzymes hydrolyze cholesteryl esters to free cholesterol and fatty acids. The levels of free cholesterol and cholesteryl esters are regulated with the help of neutral cholesteryl ester hydrolase, which converts cholesteryl ester to free cholesterol. After cholesterol leaves the lysosome, it is transported to the ER and to the plasma membrane by means of an intermediate step through the Golgi apparatus. Recycling compartments, especially multivesicular endosomes, harbor most of the cholesterol in the endocytic pathway. The intra-endosomal membranes of multivesicular late endosomes that are enriched in the phospholipids lyso-bisphosphatidic acid/bismonoacylglycerophosphate serve as important regulators of cholesterol transport (Kobayashi et al. 1999 Ikonen 2008). Lysobisphosphatidic acid is structurally... 

The initial steps of reverse cholesterol transport involve export of cholesterol from peripheral cells to plasma lipoproteins for subsequent delivery to the liver. In vivo, HDL or its apolipoproteins act as acceptors of cholesterol from peripheral cells, carrying it to the liver for degradation. When cholesterol acceptors such as HDL are present, cholesterol efflux from macrophages is accelerated, which prevents foam cell formation. To produce this efflux, neutral cholesteryl ester hydrolase catalyzes intracellular hydrolysis of cholesteryl esters into free cholesterol in the lysosome (Avart et al. 1999). 

At a later stage (10-18 days) cellular infiltration is usually extensive and clinical symptoms of the disease are overt. Lysosomal permeability, and hydrolase, and neutral proteinase activity are markedly accentuated [120]. Soluble breiin proteins at this stage are decreased [122]. Myelin lipid synthesis, as measured by glucose uptake, remains below normal while that of protein increases. In the non-myelin fraction, however, both of these metabolic activities are intensified [121]. The latter may be ascribed to the invading inflammatory cells. These chcinges, as well as the loss of myelin seen at this stage in microscopic sections, correlate with reduction of the amount of phospholipids and cholesterol, and the appearance of cholesterol esters [123]. 

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